4.8 Article

Alternating sources of perisomatic inhibition behavior

期刊

NEURON
卷 109, 期 6, 页码 -

出版社

CELL PRESS
DOI: 10.1016/j.neuron.2021.01.003

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资金

  1. National Institute Of Neurological Disorders And Stroke of the National Institutes of Health (NINDS, NIH) [R01NS99457, U19NS104590, K99NS117795, 5F31NS110316-03, R01NS081297, 5P01NS074972, 5T32NS007280]
  2. National Institute of Mental Health (NIMH) [R01MH124047, R01MH124867, R01MH111529, UG3MH120096, R01MH071679]
  3. American Epilepsy Society Postdoctoral Research Fellowship
  4. AES Junior Investigator Award
  5. JSPS Overseas Research Fellowship
  6. Canadian Institutes of Health Research Postdoctoral Research Fellowship
  7. Simons Foundation [566615]
  8. NIH [NS069375]
  9. Allen Institute for Brain Science

向作者/读者索取更多资源

Interneurons expressing cholecystokinin (CCK) and parvalbumin (PV) play important roles in regulating hippocampal pyramidal cell output. The activity of CCK BCs in the CA1 of the mouse hippocampus scales inversely with PV and pyramidal cell activity at behaviorally relevant timescales. This inverse coupling is mediated through powerful inhibitory control of CCK BCs by PV cells, demonstrating a novel form of brain-state-specific segregation of inhibition during spontaneous behavior.
Interneurons expressing cholecystokinin (CCK) and parvalbumin (PV) constitute two key GABAergic controllers of hippocampal pyramidal cell output. Although the temporally precise and millisecond-scale inhibitory regulation of neuronal ensembles delivered by PV interneurons is well established, the in vivo recruitment patterns of CCK-expressing basket cell (BC) populations has remained unknown. We show in the CA1 of the mouse hippocampus that the activity of CCK BCs inversely scales with both PV and pyramidal cell activity at the behaviorally relevant timescales of seconds. Intervention experiments indicated that the inverse coupling of CCK and PV GABAergic systems arises through a mechanism involving powerful inhibitory control of CCK BCs by PV cells. The tightly coupled complementarity of two key microcircuit regulatory modules demonstrates a novel form of brain-state-specific segregation of inhibition during spontaneous behavior.

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