Mouse primary auditory cortex (A1) operates as an inhibition-stabilized network…

Mouse primary auditory cortex (A1) operates as an inhibition-stabilized network in the awake state: optogenetic inactivation of PV interneurons produces a paradoxical increase in inhibitory synaptic input onto pyramidal cells, evidencing strong recurrent E→E excitation.

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  "n": 0,
  "doi": "10.1016/j.neuron.2017.06.019",
  "claim": "Mouse primary auditory cortex (A1) operates as an inhibition-stabilized network in the awake state: optogenetic inactivation of PV interneurons produces a paradoxical increase in inhibitory synaptic input onto pyramidal cells, evidencing strong recurrent E→E excitation.",
  "cite_key": "Kato2017",
  "evidence": "Whole-cell voltage-clamp recordings of IPSCs in mouse A1 pyramidal cells during optogenetic inactivation of PV interneurons; paradoxical IPSC increase observed in awake mice; SOM-mediated lateral inhibition via recurrent excitation withdrawal.",
  "effect_size": "paradoxical increase in IPSCs during inhibitory inactivation (qualitative direction; full numbers in figures)",
  "text_access": "fulltext",
  "study_system": "Mouse A1, awake/anesthetized, in vivo whole-cell recording + optogenetic PV inactivation",
  "argument_role": "supporting",
  "replication_status": "independently_replicated",
  "claim_source_sentence": "However, this model fails to explain the paradoxical increase in inhibitory inputs during optogenetic inactivation of PV cells, and therefore the most parsimonious explanation is that A1 in awake brain operates as an ISN.",
  "source_provenance_status": "ok",
  "replication_evidence_dois": [
    "10.7554/eLife.54875"
  ],
  "effect_size_source_sentence": "Our observation of a paradoxical increase in IPSCs during optogenetic inactivation of inhibitory neurons further supports this model ()."
}

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Whole-cell voltage-clamp recordings of IPSCs in mouse A1 pyramidal cells during optogenetic inactivation of PV interneurons; paradoxical IPSC increase observed in awake mice; SOM-mediated lateral inhibition via recurrent excitation withdrawal.