Version history

{
  "kind": "infographic",
  "prompt": "Astrocyte Calcium Signaling figure 1",
  "provider": "other",
  "raw_fields": {
    "papers": [
      {
        "doi": "10.1038/nn.4001",
        "note": "Srinivasan 2015: somatic Ca2+ essentially absent but process Ca2+ preserved in IP3R2-/-",
        "value": "soma: essentially absent; processes: preserved",
        "compartment": "soma (primary); fine processes (secondary)",
        "measurements": [
          {
            "value": "largely abolished (qualitative)",
            "compartment": "soma",
            "value_source_sentence": "In the case of WT mouse astrocytes expressing GCaMP6f, we could readily identify somatic Ca 2+ fluctuations, whereas these were essentially absent in IP3R2 − / − astrocytes."
          },
          {
            "value": "preserved (qualitative)",
            "compartment": "fine processes",
            "value_source_sentence": "Rather, we found a rich variety of previously unknown IP3R2 independent Ca 2+ fluctuations within astrocyte processes that responded to pharmacological and sensory stimuli in brain slices and in vivo , respectively."
          }
        ],
        "value_source_sentence": "In the case of WT mouse astrocytes expressing GCaMP6f, we could readily identify somatic Ca 2+ fluctuations, whereas these were essentially absent in IP3R2 − / − astrocytes."
      },
      {
        "doi": "10.3389/fnbeh.2014.00384",
        "note": "Petravicz 2014: IP3R2-KO has normal behavior",
        "value": "behavioral tasks normal",
        "compartment": "whole-cell / behavior",
        "value_source_sentence": "We present the novel finding that behavioral processes are unaffected by lack of astrocyte IP3R-mediated Ca(2+) signals."
      },
      {
        "doi": "10.1523/jneurosci.5289-11.2011",
        "note": "Takata 2011: NBM-whisker plasticity lost in IP3R2-/-",
        "value": "plasticity abolished",
        "compartment": "somatic (cholinergic plasticity)",
        "value_source_sentence": "The elevation of astrocytic [Ca(2+)](i) is crucial in this type of synaptic plasticity, as the plasticity could not be induced in inositol-1,4,5-trisphosphate receptor type 2 knock-out (IP(3)R2-KO) mice, in which astrocytic [Ca(2+)](i) surges are diminished."
      },
      {
        "doi": "10.3390/cells14141103",
        "note": "Ye et al 2025: confirms ongoing controversy re IP3R2 phenotype",
        "value": "locomotion-evoked process Ca2+ reduced",
        "compartment": "process/sensory-evoked",
        "value_source_sentence": "We report that vS1 astrocytic Ca<sup>2+</sup> elevation in both wild-type and <i>Itpr2</i><sup>-/-</sup> mice was significantly modulated by free whisking and locomotion."
      }
    ],
    "axis_label": "Fraction of astrocyte Ca2+ activity remaining in Itpr2-/- (%)",
    "comparison_topic": "Effect of Itpr2 (IP3R2) genetic deletion on astrocyte Ca2+ signals, broken down by subcellular compartment"
  },
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  "source_refs": [
    "paper:paper-29a722660e41",
    "paper:paper-5e6adeb1c300",
    "paper:paper-9c595c660d61",
    "paper:paper-883c8368100c"
  ],
  "section_title": "Astrocyte Calcium Signaling",
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}