Source:http://linkedlifedata.com/resource/pubmed/id/17959799
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rdf:type | |
lifeskim:mentions |
umls-concept:C0020663,
umls-concept:C0027882,
umls-concept:C0065898,
umls-concept:C0079883,
umls-concept:C0439831,
umls-concept:C0439851,
umls-concept:C0549255,
umls-concept:C0871261,
umls-concept:C1152715,
umls-concept:C1514758,
umls-concept:C1552596,
umls-concept:C1627358,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C1947931,
umls-concept:C2349975,
umls-concept:C2911692
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pubmed:issue |
43
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pubmed:dateCreated |
2007-10-25
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pubmed:abstractText |
The effect of group I metabotropic glutamate receptor (mGluR1 and mGluR5) activation on identified melanin-concentrating hormone (MCH) neurons was studied using patch-clamp recording in hypothalamic slices from green fluorescent protein-expressing transgenic mice. S-3,5-dihydroxyphenylglycine (DHPG), a selective group I mGluR agonist, depolarized MCH cells and increased spike frequency. The mGluR-mediated depolarization was not blocked with tetrodotoxin but was significantly reduced by replacement of extracellular Na+ with Tris, by Ni2+ or the Na+/Ca2+ exchanger blocker KB-R7943, or with BAPTA in the pipette, consistent with a mechanism based on activation of the Na+/Ca2+ exchanger. DHPG also decreased potassium currents. DHPG-induced depolarization was reduced by either mGluR1 or mGluR5 antagonists, suggesting involvement of both receptor subtypes. DHPG-induced depolarization desensitized; blockade of mGluR1 prevented the desensitization. Group I mGluR activation enhanced NMDA-evoked currents; this enhancement was remarkably long lasting and could be blocked by protein kinase A or C blockers. DHPG potentiated electrically evoked NMDA receptor-mediated postsynaptic currents, and mGluR5 antagonists blocked this action. Group I mGluRs increased spontaneous EPSCs in MCH neurons, possibly by stimulation of nearby mGluR-expressing hypocretin neurons. We found no tonic activation of mGluRs. However, electrical stimulation produced a slow inward current, which could be blocked by group I mGluR antagonists, suggesting high, but not low, levels of synaptically released glutamate activated mGluRs. Together, group I mGluRs increase MCH neuron activity by multiple presynaptic and postsynaptic mechanisms, suggesting mGluRs may therefore play a role in hypothalamic signaling relating to MCH neuron modulation of food intake and energy metabolism.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Hypothalamic Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Melanins,
http://linkedlifedata.com/resource/pubmed/chemical/N-Methylaspartate,
http://linkedlifedata.com/resource/pubmed/chemical/Pituitary Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Metabotropic Glutamate,
http://linkedlifedata.com/resource/pubmed/chemical/melanin-concentrating hormone,
http://linkedlifedata.com/resource/pubmed/chemical/metabotropic glutamate receptor...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1529-2401
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
24
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pubmed:volume |
27
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
11560-72
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17959799-Animals,
pubmed-meshheading:17959799-Excitatory Amino Acid Antagonists,
pubmed-meshheading:17959799-Humans,
pubmed-meshheading:17959799-Hypothalamic Hormones,
pubmed-meshheading:17959799-Hypothalamus,
pubmed-meshheading:17959799-Melanins,
pubmed-meshheading:17959799-Mice,
pubmed-meshheading:17959799-Mice, Transgenic,
pubmed-meshheading:17959799-N-Methylaspartate,
pubmed-meshheading:17959799-Neurons,
pubmed-meshheading:17959799-Pituitary Hormones,
pubmed-meshheading:17959799-Receptors, Metabotropic Glutamate,
pubmed-meshheading:17959799-Synaptic Transmission,
pubmed-meshheading:17959799-Time Factors
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pubmed:year |
2007
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pubmed:articleTitle |
Rapid direct excitation and long-lasting enhancement of NMDA response by group I metabotropic glutamate receptor activation of hypothalamic melanin-concentrating hormone neurons.
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pubmed:affiliation |
Department of Neurosurgery, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, N.I.H., Extramural
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