Document Detail


Inhibition of dendritic calcium influx by activation of G-protein-coupled receptors in the hippocampus.
MedLine Citation:
PMID:  9405566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein-coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 microM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein-mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.
Authors:
H Chen; N A Lambert
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of neurophysiology     Volume:  78     ISSN:  0022-3077     ISO Abbreviation:  J. Neurophysiol.     Publication Date:  1997 Dec 
Date Detail:
Created Date:  1998-02-05     Completed Date:  1998-02-05     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0375404     Medline TA:  J Neurophysiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3484-8     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912-2300, USA.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / physiology
Animals
Calcium / metabolism*
Dendrites / metabolism*
GTP-Binding Proteins / physiology*
Hippocampus / metabolism*
Potassium Channels / physiology
Pyramidal Cells / ultrastructure
Rats
Rats, Sprague-Dawley
Receptors, Cell Surface / physiology*
Grant Support
ID/Acronym/Agency:
NS-36455/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels; 0/Receptors, Cell Surface; 7440-70-2/Calcium; EC 3.6.1.-/GTP-Binding Proteins

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


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