Document Detail


Separate signalling mechanisms underlie mGluR1 modulation of leak channels and NMDA receptors in the network underlying locomotion.
MedLine Citation:
PMID:  19403613     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Metabotropic glutamate receptor subtype 1 (mGluR1) contributes importantly to the activity of the spinal locomotor network. For example, it potentiates NMDA current and inhibits leak conductance in lamprey spinal cord neurons. In this study we examined the signalling pathways underlying the mGluR1 modulation of NMDA receptors and leak channels, respectively. Our results show that mGluR1-induced potentiation of NMDA current required activation of phospholipase C (PLC) and was independent of the increase in the intracellular Ca2+ concentration because it was unaffected by the Ca2+ chelator BAPTA and by depletion of the internal Ca2+ stores with thapsigargin. We also show that the mGluR1-mediated inhibition of leak channels is mediated by activation of G-proteins. Finally, we show that blockade of protein kinase C (PKC) abolished the mGluR1-induced inhibition of leak current without affecting the potentiation of NMDA receptors. The contribution of mGluR1-mediated modulation of leak channels to the potentiation of the locomotor cycle frequency was assessed during fictive locomotion. Blockade of PKC significantly decreased the short-term potentiation of locomotor cycle frequency by mGluR1. These results show that the effects of mGluR1 activation on the two cellular targets, the NMDA receptor and leak channels, are mediated through separate signalling pathways.
Authors:
Evanthia Nanou; Alexandros Kyriakatos; Petronella Kettunen; Abdeljabbar El Manira
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-04-29
Journal Detail:
Title:  The Journal of physiology     Volume:  587     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2009 Jun 
Date Detail:
Created Date:  2009-06-15     Completed Date:  2009-09-21     Revised Date:  2010-09-24    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  3001-8     Citation Subset:  IM    
Affiliation:
Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Animals
GTP-Binding Proteins / physiology
Lampreys / physiology*
Locomotion / physiology*
Long-Term Potentiation / physiology
Methoxyhydroxyphenylglycol / analogs & derivatives,  pharmacology
Nerve Net / physiology*
Neuronal Plasticity / physiology
Patch-Clamp Techniques
Protein Kinase C / physiology
Receptors, Metabotropic Glutamate / physiology*
Receptors, N-Methyl-D-Aspartate / physiology*
Spinal Cord / physiology
Type C Phospholipases / physiology
Chemical
Reg. No./Substance:
0/Receptors, Metabotropic Glutamate; 0/Receptors, N-Methyl-D-Aspartate; 0/metabotropic glutamate receptor type 1; 3343-19-9/dihydroxyphenylethylene glycol; 534-82-7/Methoxyhydroxyphenylglycol; EC 2.7.11.13/Protein Kinase C; EC 3.1.4.-/Type C Phospholipases; EC 3.6.1.-/GTP-Binding Proteins
Comments/Corrections

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


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