Send to

Choose Destination
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

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.
U.O. of Neurophysiopathology and Diagnostic Epileptology, Foundation Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Neurological Institute Carlo Besta, Milano, Italy.
U.O. of Clinical Epileptology and Experimental Neurophysiology, Foundation Istituto di Ricerca e Cura a Carattere Scientifico (IRCCS) Neurological Institute Carlo Besta, Milano, Italy.
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.
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.


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.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center