Benchmarking optogenetic inactivation methods in mouse neocortex shows that GAB…

Benchmarking optogenetic inactivation methods in mouse neocortex shows that GABAergic-neuron photoexcitation (especially via transgenic GtACR1) gives the strongest suppression, that inactivation spreads beyond the photostimulation spot due to strong cortical coupling, and that over a range of light intensities GABAergic photoexcitation paradoxically reduces inhibitory firing alongside pyramidal firing — a signature of inhibition-stabilized network operation.

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  "doi": "10.7554/elife.48622",
  "claim": "Benchmarking optogenetic inactivation methods in mouse neocortex shows that GABAergic-neuron photoexcitation (especially via transgenic GtACR1) gives the strongest suppression, that inactivation spreads beyond the photostimulation spot due to strong cortical coupling, and that over a range of light intensities GABAergic photoexcitation paradoxically reduces inhibitory firing alongside pyramidal firing — a signature of inhibition-stabilized network operation.",
  "cite_key": "Li2019",
  "evidence": "Optogenetic excitation of GABAergic neurons produced more effective inactivation than light-gated ion pumps. Transgenic mice expressing the light-dependent chloride channel GtACR1 produced the most potent inactivation. Generally, inactivation spread substantially beyond the photostimulation light, caused by strong coupling between cortical neurons. The offset of optogenetic inactivation was followed by rebound excitation in a light dose-dependent manner.",
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  "study_system": "mouse neocortex; in vivo optogenetic inactivation with calibrated light dosing and electrophysiology",
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  "claim_source_sentence": "Over some range of light intensity, optogenetic excitation of inhibitory neurons reduced activity in these neurons, together with pyramidal neurons, a signature of inhibition-stabilized neural networks ('paradoxical effect').",
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Optogenetic excitation of GABAergic neurons produced more effective inactivation than light-gated ion pumps. Transgenic mice expressing the light-dependent chloride channel GtACR1 produced the most potent inactivation. Generally, inactivation spread substantially beyond the photostimulation light, caused by strong coupling between cortical neurons. The offset of optogenetic inactivation was followed by rebound excitation in a light dose-dependent manner.