Browse

Enhancement of dendritic persistent Na+ currents by mGluR5 leads to an advancement of spike timing with an increase in temporal precision

DC Field Value Language
dc.contributor.authorYu, Weonjin-
dc.contributor.authorSohn, Jong-Woo-
dc.contributor.authorKwon, Jaehan-
dc.contributor.authorLee, Suk-Ho-
dc.contributor.authorKim, Sooyun-
dc.contributor.authorHo, Won-Kyung-
dc.date.accessioned2019-03-07T05:57:32Z-
dc.date.available2019-03-07T15:01:21Z-
dc.date.issued2018-11-09-
dc.identifier.citationMolecular Brain, 11(1):67ko_KR
dc.identifier.issn1756-6606-
dc.identifier.urihttps://hdl.handle.net/10371/146887-
dc.description.abstractTiming and temporal precision of action potential generation are thought to be important for encoding of information in the brain. The ability of single neurons to transform their input into output action potential is primarily determined by intrinsic excitability. Particularly, plastic changes in intrinsic excitability represent the cellular substrate for spatial memory formation in CA1 pyramidal neurons (CA1-PNs). Here, we report that synaptically activated mGluR5-signaling can modulate the intrinsic excitability of CA1-PNs. Specifically, high-frequency stimulation at CA3-CA1 synapses increased firing rate and advanced spike onset with an improvement of temporal precision. These changes are mediated by mGluR5 activation that induces cADPR/RyR-dependent Ca2+ release in the dendrites of CA1-PNs, which in turn causes an increase in persistent Na+ currents (INa,P) in the dendrites. When group I mGluRs in CA1-PNs are globally activated pharmacologically, afterdepolarization (ADP) generation as well as increased firing rate are observed. These effects are abolished by inhibiting mGluR5/cADPR/RyR-dependent Ca2+ release. However, the increase in firing rate, but not the generation of ADP is affected by inhibiting INa,P. The differences between local and global activation of mGluR5-signaling in CA1-PNs indicates that mGluR5-dependent modulation of intrinsic excitability is highly compartmentalized and a variety of ion channels are recruited upon their differential subcellular localizations. As mGluR5 activation is induced by physiologically plausible brief high-frequency stimulation at CA3-CA1 synapses, our results suggest that mGluR5-induced enhancement of dendritic INa,P in CA1-PNs may provide important implications for our understanding about place field formation in the hippocampus.ko_KR
dc.description.sponsorshipThis work was supported by the National Research Foundation of Korea (NRF-2010-0027941 and NRF-2017R1A2B2010186 to W-K.H., and NRF2018R1D1A1B07046742 to S.K.). W.Y. and J.K recieved a scholarship from the BK21-plus program.ko_KR
dc.language.isoenko_KR
dc.publisherBioMed Centralko_KR
dc.subjectmGluR5-dependent plasticityko_KR
dc.subjectPersistent sodium currentko_KR
dc.subjectCA1 pyramidal neuronsko_KR
dc.subjectIntrinsic excitabilityko_KR
dc.titleEnhancement of dendritic persistent Na+ currents by mGluR5 leads to an advancement of spike timing with an increase in temporal precisionko_KR
dc.typeArticleko_KR
dc.identifier.doi10.1186/s13041-018-0410-7-
dc.language.rfc3066en-
dc.rights.holderThe Author(s).-
dc.date.updated2018-11-11T06:32:52Z-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Neuroscience (뇌신경과학전공)Journal Papers (저널논문_뇌신경과학전공)
College of Medicine/School of Medicine (의과대학/대학원)Dept. of Physiology (생리학교실)Journal Papers (저널논문_생리학교실)
Files in This Item:
  • mendeley

Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse