Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
2000-7-26
pubmed:abstractText
The loss of dopaminergic innervation of the basal ganglia, a group of subcortical regions involved in motor control, is the hallmark of Parkinson's disease. The resulting molecular and cellular alterations mediate behavioral deficits and may modify neuronal responses to other neurotransmitters. In the present study, we sought to determine the effects of chronic dopamine (DA) depletion on responses mediated by stimulation of serotonergic 2C (5-HT(2C)) receptors, a serotonergic receptor subtype present in discrete regions of the basal ganglia. Specifically, the effects of unilateral lesions of nigrostriatal DA neurons on oral dyskinesia and Fos protein expression induced by the non-selective 5-HT(2C) agonist 1-(m-chlorophenyl)piperazine (m-CPP) were examined. Confirming previous findings, both peripheral and local injections of m-CPP into the subthalamic nucleus elicited oral dyskinesia. Nigrostriatal lesions markedly enhanced oral bouts induced by peripheral but not intrasubthalamic administration of m-CPP. In intact rats, Fos expression was increased by m-CPP (1 mg/kg, i.p.) in the striatum and the subthalamic nucleus. After nigrostriatal lesions, m-CPP-induced Fos expression remained unchanged in the subthalamic nucleus but was reduced in the medial quadrants of the striatum and was markedly enhanced in the entopeduncular nucleus. These data demonstrate regionally specific alterations in behavioral and cellular responses to a serotonergic agonist in an animal model of Parkinson's disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5170-8
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10864974-Animals, pubmed-meshheading:10864974-Corpus Striatum, pubmed-meshheading:10864974-Dopamine, pubmed-meshheading:10864974-Dyskinesia, Drug-Induced, pubmed-meshheading:10864974-Gene Expression Regulation, pubmed-meshheading:10864974-Genes, fos, pubmed-meshheading:10864974-Male, pubmed-meshheading:10864974-Motor Activity, pubmed-meshheading:10864974-Neurons, pubmed-meshheading:10864974-Oxidopamine, pubmed-meshheading:10864974-Piperazines, pubmed-meshheading:10864974-Proto-Oncogene Proteins c-fos, pubmed-meshheading:10864974-Rats, pubmed-meshheading:10864974-Rats, Sprague-Dawley, pubmed-meshheading:10864974-Receptor, Serotonin, 5-HT2C, pubmed-meshheading:10864974-Receptors, Serotonin, pubmed-meshheading:10864974-Serotonin Receptor Agonists, pubmed-meshheading:10864974-Substantia Nigra, pubmed-meshheading:10864974-Thalamic Nuclei, pubmed-meshheading:10864974-Tyrosine 3-Monooxygenase
pubmed:year
2000
pubmed:articleTitle
Nigrostriatal lesions alter oral dyskinesia and c-Fos expression induced by the serotonin agonist 1-(m-chlorophenyl)piperazine in adult rats.
pubmed:affiliation
Department of Neurology, University of California, Los Angeles School of Medicine, Los Angeles, California 90095, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.