Version history

{
  "field_tag": "astrocytes",
  "text": "What resolves this contention: Mechanistic conflict: one line of evidence concludes that astrocytic Ca2+ is dispensable for synaptic transmission based on IP3R2 KO, while another shows that IP3R2-independent TRPA1-mediated microdomain Ca2+ in astrocytes is required for basal D-serine supply and thus LTP. / IP3R2 is the key astrocytic IP3R driving Gq-linked GPCR-mediated Ca2+ increases in hippocampal astrocytes, and removal of IP3R2-dependent astrocytic Ca2+ does not significantly affect excitatory neuronal synaptic activity or ambient glutamate levels. / Independent TRPA1 channel-mediated Ca2+ flux in astrocytes (not dependent on IP3R2) maintains basal astrocytic Ca2+ and drives constitutive D-serine release that supports Schaffer collateral–CA1 LTP; pharmacological or genetic block of astrocyte TRPA1 impairs LTP.",
  "source_refs": [
    "paper:paper-778045e57b0f",
    "paper:paper-bd699ea0aec5",
    "wiki_page:computationalreviewastrocytes-08",
    "paper:paper-778045e57b0f",
    "paper:paper-bd699ea0aec5",
    "wiki_page:computationalreviewastrocytes-08",
    "paper:paper-778045e57b0f",
    "paper:paper-bd699ea0aec5",
    "wiki_page:computationalreviewastrocytes-08",
    "paper:paper-778045e57b0f",
    "paper:paper-bd699ea0aec5",
    "wiki_page:computationalreviewastrocytes-08"
  ],
  "importance": "0.7200",
  "tractability": "0.5500",
  "potential_impact": "0.7000",
  "composite_score": "0.2772",
  "elo_rating": "1500.00",
  "state": "open",
  "decay_rate": "0.01000",
  "resolution_evidence_refs": []
}