Research article summary (published 27 Apr 2009):

Separate signalling mechanisms underlie mGluR1 modulation of leak channels and NMDA receptors in the network underlying locomotion.

Full Abstract

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.

Author information

Author/s: Nanou, Evanthia (E); Kyriakatos, Alexandros (A); Kettunen, Petronella (P); El Manira, Abdeljabbar (A);

Affiliation: Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: The Journal of physiology (J Physiol), published in England. (Language: eng)

Reference: 2009-Jun; vol 587 (issue Pt 12) : pp 3001-8

Dates: Created 2009/06/15; Completed 2009/09/21;

PMID: 19403613, status: MEDLINE (last retrieval date: 9/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

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

Associated Chemicals: Receptors, Metabotropic Glutamate (0) ; Receptors, N-Methyl-D-Aspartate (0) ; metabotropic glutamate receptor type 1 (0) ; dihydroxyphenylethylene glycol (3343-19-9) ; Methoxyhydroxyphenylglycol (534-82-7) ; Protein Kinase C (EC 2.7.11.13) ; Type C Phospholipases (EC 3.1.4.-) ; GTP-Binding Proteins (EC 3.6.1.-)

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