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PLoS Biol. 2014 Sep 9;12(9):e1001944. doi: 10.1371/journal.pbio.1001944. eCollection 2014 Sep.

Action potential initiation in neocortical inhibitory interneurons.

Author information

1
Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, and University of Chinese Academy of Sciences, Shanghai, China.
2
U.O. of Neurophysiopathology and Diagnostic Epileptology, Foundation Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Neurological Institute Carlo Besta, Milano, Italy.
3
U.O. of Clinical Epileptology and Experimental Neurophysiology, Foundation Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Neurological Institute Carlo Besta, Milano, Italy.
4
Institute of Molecular and Cellular Pharmacology (IPMC), Laboratory of Excellence Ion Channel Science and Therapeutics (LabEx ICST), CNRS UMR7275 and University of Nice-Sophia Antipolis, Valbonne, France.
5
State Key Laboratory of Cognitive Neuroscience and Learning and IDG/McGovern Institute for Brain Research, School of Brain and Cognitive Sciences, Beijing Normal University, Beijing, China; Center for Collaboration and Innovation in Brain and Learning Sciences, Beijing Normal University, Beijing, China.

Abstract

Action potential (AP) generation in inhibitory interneurons is critical for cortical excitation-inhibition balance and information processing. However, it remains unclear what determines AP initiation in different interneurons. We focused on two predominant interneuron types in neocortex: parvalbumin (PV)- and somatostatin (SST)-expressing neurons. Patch-clamp recording from mouse prefrontal cortical slices showed that axonal but not somatic Na+ channels exhibit different voltage-dependent properties. The minimal activation voltage of axonal channels in SST was substantially higher (∼7 mV) than in PV cells, consistent with differences in AP thresholds. A more mixed distribution of high- and low-threshold channel subtypes at the axon initial segment (AIS) of SST cells may lead to these differences. Surprisingly, NaV1.2 was found accumulated at AIS of SST but not PV cells; reducing NaV1.2-mediated currents in interneurons promoted recurrent network activity. Together, our results reveal the molecular identity of axonal Na+ channels in interneurons and their contribution to AP generation and regulation of network activity.

PMID:
25203314
PMCID:
PMC4159120
DOI:
10.1371/journal.pbio.1001944
[Indexed for MEDLINE]
Free PMC Article

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