| Separate signalling mechanisms underlie mGluR1 modulation of leak channels and NMDA receptors in the network underlying locomotion. | |
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MedLine Citation:
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PMID: 19403613 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Evanthia Nanou; Alexandros Kyriakatos; Petronella Kettunen; Abdeljabbar El Manira |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-04-29 |
Journal Detail:
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Title: The Journal of physiology Volume: 587 ISSN: 1469-7793 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2009 Jun |
Date Detail:
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Created Date: 2009-06-15 Completed Date: 2009-09-21 Revised Date: 2010-09-24 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 3001-8 Citation Subset: IM |
Affiliation:
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Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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 | |
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