Document Detail


Calcium-dependent isoforms of protein kinase C mediate glycine-induced synaptic enhancement at the calyx of Held.
MedLine Citation:
PMID:  23035091     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Depolarization of presynaptic terminals that arises from activation of presynaptic ionotropic receptors, or somatic depolarization, can enhance neurotransmitter release; however, the molecular mechanisms mediating this plasticity are not known. Here we investigate the mechanism of this enhancement at the calyx of Held synapse, in which presynaptic glycine receptors depolarize presynaptic terminals, elevate resting calcium levels, and potentiate release. Using knock-out mice of the calcium-sensitive PKC isoforms (PKC(Ca)), we find that enhancement of evoked but not spontaneous synaptic transmission by glycine is mediated primarily by PKC(Ca). Measurements of calcium at the calyx of Held indicate that deficits in synaptic modulation in PKC(Ca) knock-out mice occur downstream of presynaptic calcium increases. Glycine enhances synaptic transmission primarily by increasing the effective size of the pool of readily releasable vesicles. Our results reveal that PKC(Ca) can enhance evoked neurotransmitter release in response to calcium increases caused by small presynaptic depolarizations.
Authors:
YunXiang Chu; Diasynou Fioravante; Monica Thanawala; Michael Leitges; Wade G Regehr
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  32     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-04     Completed Date:  2013-01-17     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  13796-804     Citation Subset:  IM    
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Calcium Signaling / drug effects,  physiology*
Cochlear Nucleus / enzymology*,  physiology,  ultrastructure
Electric Stimulation
Excitatory Postsynaptic Potentials / drug effects,  physiology
Female
Glycine / pharmacology*
Long-Term Potentiation / drug effects*
Male
Mice
Mice, Knockout
Nerve Tissue Proteins / physiology*
Presynaptic Terminals / drug effects,  physiology
Protein Kinase C / deficiency,  genetics,  physiology*
Protein Kinase C beta
Protein Kinase C-alpha / deficiency,  genetics,  physiology*
Strychnine / pharmacology
Synapses / drug effects,  enzymology*,  physiology
Grant Support
ID/Acronym/Agency:
R01 NS032405/NS/NINDS NIH HHS; R37 NS032405/NS/NINDS NIH HHS; T32 MH020017/MH/NIMH NIH HHS; //Howard Hughes Medical Institute
Chemical
Reg. No./Substance:
0/Nerve Tissue Proteins; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/Protein Kinase C beta; EC 2.7.11.13/Protein Kinase C-alpha; H9Y79VD43J/Strychnine; TE7660XO1C/Glycine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Acetylcholine facilitates recovery of episodic memory after brain damage.
Next Document:  Effects of decision variables and intraparietal stimulation on sensorimotor oscillatory activity in ...