Source:http://linkedlifedata.com/resource/pubmed/id/11267640
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2001-3-27
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pubmed:abstractText |
Peripheral administration of the 5-hydroxytryptamine (5-HT)(2C/1B) agonist 1-(m-chlorophenyl)piperazine (m-CPP) produces abnormal orofacial movements in rats. We have previously shown that this behavior is mediated by 5-HT(2C) receptors in the subthalamic nucleus [Neuroscience 72 (1996) 117]. The present studies examined this effect after serotonin depletion to determine whether removal of endogenous serotonin affected this behavioral response and/or subthalamic 5-HT(2C) receptors. Rats received an intraventricular infusion of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT, 100 mg/10 ml) or vehicle after desipramine pretreatment (25 mg/kg ip). The efficacy of serotonin depletion was confirmed by a decrease in serotonin uptake sites measured by autoradiography. Oral dyskinesia induced by peripheral administration of m-CPP (1.0 mg/kg ip) was markedly increased in lesioned rats compared to sham-operated controls 4 and 8 but not 12 days after the lesion. A subset of lesioned rats that displayed transient seizures after m-CPP injection did not prevent the measurement of oral dyskinesia during the observation period. No differences in 5-HT(2C) receptor levels were found with ligand-binding autoradiography in the subthalamic nucleus, or in other brain regions that express this receptor, in rats sacrificed 5 days following 5,7-DHT lesions. The data indicate that lesion of serotonergic neurons in adult rats induces a transient increase in motor responses mediated by subthalamic 5-HT(2C) receptors. These data suggest that functional alterations in serotonergic transmission in the subthalamic nucleus may be involved in the pathophysiology of hyperkinetic movement disorders.
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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/1-(3-chlorophenyl)piperazine,
http://linkedlifedata.com/resource/pubmed/chemical/5,7-Dihydroxytryptamine,
http://linkedlifedata.com/resource/pubmed/chemical/Piperazines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Serotonin, 5-HT2C,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Serotonin,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Serotonin Receptor Agonists
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0091-3057
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
347-53
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11267640-5,7-Dihydroxytryptamine,
pubmed-meshheading:11267640-Animals,
pubmed-meshheading:11267640-Behavior, Animal,
pubmed-meshheading:11267640-Dyskinesia, Drug-Induced,
pubmed-meshheading:11267640-Male,
pubmed-meshheading:11267640-Piperazines,
pubmed-meshheading:11267640-Rats,
pubmed-meshheading:11267640-Rats, Sprague-Dawley,
pubmed-meshheading:11267640-Receptor, Serotonin, 5-HT2C,
pubmed-meshheading:11267640-Receptors, Serotonin,
pubmed-meshheading:11267640-Serotonin Agents,
pubmed-meshheading:11267640-Serotonin Receptor Agonists,
pubmed-meshheading:11267640-Subthalamic Nucleus
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pubmed:year |
2001
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pubmed:articleTitle |
Increased m-CPP-induced oral dyskinesia after lesion of serotonergic neurons.
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pubmed:affiliation |
Department of Neurology, UCLA School of Medicine, Los Angeles, CA 90095, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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