Astrocytes in Synaptic Plasticity

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Citation anchors captured: 104

Citation contexts

^{1Citationpaper:paper-4c0b69613ffbIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference} If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...
^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference} If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...
^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference} If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...
^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference} If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference} If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference} The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference} first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference} extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference} The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference} first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}0 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}1 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}2 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}3 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}4 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}5 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}6 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}7 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}8 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{2Citationpaper:paper-5ced9eaa871aIf network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}9 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}0 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}1 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}2 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}3 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}4 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}5 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}6 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}7 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}8 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{3Citationpaper:paper-05bd7b9585c9If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}9 The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}0 first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}1 extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...
^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}2 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}3. The same logic underlies rescue experiments in...
^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}4 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}5. The same logic underlies rescue experiments in...
^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}6 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}7. The same logic underlies rescue experiments in...
^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}8 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{4Citationpaper:paper-2c57c11cf566If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}9. The same logic underlies rescue experiments in...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}0 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}1. The same logic underlies rescue experiments in...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}2 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}3. The same logic underlies rescue experiments in...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}4 The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $\sim$ 150,% to $\sim$ 183,% of baseline ( $n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions ^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}5. The same logic underlies rescue experiments in...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}6 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}7 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}8 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{5Citationpaper:paper-2ea9ef87bc30If network-level gap-junctional coupling (Section {ref}sec:gap-junctions-networks) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...content/08_plasticity_modulation.md:line 4Open reference}9 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}0 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}1 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}2 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}3 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}4 The source of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}5 LTP magnitude across astrocyte Ca $^{2+}$ /gliotransmission manipulations in hippocampal CA1, shown as two separate panels on native scales rather than a single shared-axis bar chart. (A) Single-astrocyte D-serine depletion (intra-astrocyte HOAsp) reduces fEPSP % change from $52\pm11$ to $12\pm11$ in acute mouse slice ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}6. (B) Gain-of-function / co-agonist-saturation manipulations plotted on...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}7 LTP magnitude across astrocyte Ca $^{2+}$ /gliotransmission manipulations in hippocampal CA1, shown as two separate panels on native scales rather than a single shared-axis bar chart. (A) Single-astrocyte D-serine depletion (intra-astrocyte HOAsp) reduces fEPSP % change from $52\pm11$ to $12\pm11$ in acute mouse slice ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}8. (B) Gain-of-function / co-agonist-saturation manipulations plotted on...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}9 LTP magnitude across astrocyte Ca $^{2+}$ /gliotransmission manipulations in hippocampal CA1, shown as two separate panels on native scales rather than a single shared-axis bar chart. (A) Single-astrocyte D-serine depletion (intra-astrocyte HOAsp) reduces fEPSP % change from $52\pm11$ to $12\pm11$ in acute mouse slice ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}0. (B) Gain-of-function / co-agonist-saturation manipulations plotted on...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}1 If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca $^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}2 showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca $^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}3 If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca $^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}4 showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca $^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}5 If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca $^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}6 showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca $^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}7 If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca $^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}8 showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca $^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}9 If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca $^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}0 showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca $^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}1 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}2 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}3 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}4 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}5 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}6 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}7 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}8 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}9 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}0 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}1 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}2 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}3 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}4 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}5 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}6 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}7 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}8 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{7Citationpaper:paper-5525e0e4dcd1The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}9 The two positions are not fully reconcilable, but several partial resolutions have emerged. First, ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}0 showed that IP3R2 is not the only route to astrocytic Ca $^{2+}$ : TRPA1 contributes a tonic, resting Ca $^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}1 Chemogenetics has made it possible to translate these slice-level arguments into behavioural tests. The effects are large but the sign and replicability depend on the manipulation (Fig. {ref}fig:sec8-memory-manipulations). ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}2 reported that activating astrocytic Gq-DREADDs in CA1 during contextual fear acquisition raised subsequent contextual freezing by $\sim$ 40% (chemogenetic) and $\sim$ 89% (optogene...
^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}3 Chemogenetics has made it possible to translate these slice-level arguments into behavioural tests. The effects are large but the sign and replicability depend on the manipulation (Fig. {ref}fig:sec8-memory-manipulations). ^{6Citationpaper:paper-926b7ae9f5edThe best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang2003procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger2010nature] extended the claim to acute slice: depleting D-serine from a single patched astrocyte by intracellular HOAsp loading collapsed...content/08_plasticity_modulation.md:line 8Open reference}4 reported that activating astrocytic Gq-DREADDs in CA1 during contextual fear acquisition raised subsequent contextual freezing by $\sim$ 40% (chemogenetic) and $\sim$ 89% (optogene...
... 54 additional anchors in refs_json

References

[araque_2014_neuron] paper:paper-4c0b69613ffb “If network-level gap-junctional coupling (Section {ref}`sec:gap-junctions-networks`) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...”
[halassa_2010_annurev] paper:paper-5ced9eaa871a “If network-level gap-junctional coupling (Section {ref}`sec:gap-junctions-networks`) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...”
[durkee_2021_trendsneurosciences] paper:paper-05bd7b9585c9 “If network-level gap-junctional coupling (Section {ref}`sec:gap-junctions-networks`) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...”
[verkhratsky_2018_physiological] paper:paper-2c57c11cf566 “If network-level gap-junctional coupling (Section {ref}`sec:gap-junctions-networks`) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...”
[goenaga_2023_frontsynaptic] paper:paper-2ea9ef87bc30 “If network-level gap-junctional coupling (Section {ref}`sec:gap-junctions-networks`) is one substrate through which astrocytes shape the circuits in which they sit, local synaptic mechanisms are the other. At tripartite synapses, astrocytic processes are close enough to the cleft to release and take up neuroactive molecules on the timescale of plasticity induction, and reviews of this literature converge on a short...”
[yang_2003_procnatl] paper:paper-926b7ae9f5ed “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[henneberger_2010_nature] paper:paper-5525e0e4dcd1 “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[papouin_2017_neuron] paper:paper-5bf4b837dd32 “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[papouin_2017_philtrans] paper:paper-06005307eb50 “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[papouin_2012_cell] paper:paper-4924de7a3041 “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[shigetomi_2013_neuroscience] paper:paper-bd699ea0aec5 “The best-characterised astrocyte–plasticity link runs through D-serine at the NMDAR co-agonist (glycine) site. [yang_2003_procnatl] first argued that astrocyte-derived D-serine gates LTP induction in cultured hippocampal neurons grown on astrocyte monolayers, and [henneberger_2010_nature] extended the claim to acute slice: depleting D-serine from a *single* patched astrocyte by intracellular HOAsp loading collapsed...”
[vestring_2024_translpsychiatry] paper:paper-0685af1d3f41 “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[han_2013_cellstem] paper:paper-c0990b7b4903 “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[balu_2019_neurobiologydisease] paper:paper-04c705b2d7ad “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[benneyworth_2012_cellmol] paper:paper-375cd2fdb238 “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[benachour_2010_neurochemistry] paper:paper-ba06d7cd948b “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[rose_2018_frontmol] paper:paper-e3fcbfafbe9a “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[diniz_2012_biologicalchemistry] paper:paper-9df56c7c4fb5 “The quantitative co-agonist dependence is reinforced by a positive pharmacological control: saturating the NMDAR glycine site with bath D-cycloserine raised CA1 LTP magnitude from $∼$150\,\% to $∼$183\,\% of baseline ($n=8$ slices), indicating that endogenous co-agonist availability is sub-saturating under standard induction conditions [vestring_2024_translpsychiatry]. The same logic underlies rescue experiments in...”
[rosenberg_2013_jneurosci] paper:paper-b61c21702bde “The *source* of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...”
[wolosker_2016_trendsneurosciences] paper:paper-f5cc394cbcee “The *source* of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...”
[balu_2014_cellmol] paper:paper-b1d06baddd84 “The *source* of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...”
[neame_2019_procnatl] paper:paper-b99b42fbb5a0 “The *source* of that D-serine, however, is the first major conflict in this literature. A line of immunohistochemical and conditional-knockout work in adult tissue localises serine racemase and D-serine predominantly to neurons rather than astrocytes, and shows that neuronal release via the Asc-1 transporter is sufficient to support NMDAR-dependent transmission and LTP [rosenberg_2013_jneurosci,wolosker_2016_trendsn...”
[adamsky_2018_cell] paper:paper-79c338afafe0 “LTP magnitude across astrocyte Ca$^{2+}$/gliotransmission manipulations in hippocampal CA1, shown as two separate panels on native scales rather than a single shared-axis bar chart. **(A)** Single-astrocyte D-serine depletion (intra-astrocyte HOAsp) reduces fEPSP \% change from $52±11$ to $12±11$ in acute mouse slice [henneberger_2010_nature]. **(B)** Gain-of-function / co-agonist-saturation manipulations plotted on...”
[petravicz_2008_jneurosci] paper:paper-778045e57b0f “If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca$^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. [petravicz_2008_jneurosci] showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca$^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...”
[petravicz_2014_frontbehav] paper:paper-9c595c660d61 “If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca$^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. [petravicz_2008_jneurosci] showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca$^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...”
[agulhon_2012_frontpharmacol] paper:paper-69c21d3ca6d7 “If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca$^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. [petravicz_2008_jneurosci] showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca$^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...”
[fiacco_2018_jneurosci] paper:paper-1da111dc048d “If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca$^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. [petravicz_2008_jneurosci] showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca$^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...”
[savtchouk_2018_jneurosci] paper:paper-930310f9ad4c “If gliotransmission gates LTP, then blocking Gq-dependent astrocytic Ca$^{2+}$ rises should block plasticity. The prediction failed in a series of conditional IP3R2 knockouts. [petravicz_2008_jneurosci] showed that genetic loss of IP3R2 — the dominant astrocytic IP3 receptor — abolished GPCR-evoked astrocytic Ca$^{2+}$ responses without affecting baseline Schaffer collateral–CA1 synaptic transmission or ambient glut...”
[perezalvarez_2014_neuroscience] paper:paper-485a94449c79 “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[lalo_2018_frontmol] paper:paper-79a5bdf5ea8a “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[covelo_2018_elife] paper:paper-6a0da6de0163 “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[perea_2014_natcommun] paper:paper-2c354e126cc2 “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[bernardinelli_2014_neuralplasticity] paper:paper-8cf019918a97 “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[henneberger_2020_neuron] paper:paper-f2c64f4579f9 “The two positions are not fully reconcilable, but several partial resolutions have emerged. First, [shigetomi_2013_neuroscience] showed that IP3R2 is not the only route to astrocytic Ca$^{2+}$: TRPA1 contributes a tonic, resting Ca$^{2+}$ influx that maintains D-serine availability and LTP in a manner invisible to IP3R2 deletion. Second, a family of compartment-specific imaging and manipulation studies has revealed...”
[kol_2020_natneurosci] paper:paper-d31b944234b2 “Chemogenetics has made it possible to translate these slice-level arguments into behavioural tests. The effects are large but the sign and replicability depend on the manipulation (Fig. {ref}`fig:sec8-memory-manipulations`). [adamsky_2018_cell] reported that activating astrocytic Gq-DREADDs in CA1 during contextual fear acquisition raised subsequent contextual freezing by $∼$40\% (chemogenetic) and $∼$89\% (optogene...”

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