Linked Life Data

17255465

Source:http://linkedlifedata.com/resource/pubmed/id/17255465

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-3-19
pubmed:abstractText
Cholinergic muscarinic systems have been shown to influence dopaminergic function in the central nervous system. In addition, previous studies of benztropine analogs that inhibit dopamine uptake and show antagonism at muscarinic receptors show these drugs to be less effective than cocaine in producing its various prototypic effects such as locomotor stimulation. Because previous pharmacological studies on these topics have used nonselective M1 antagonists, we examined the interactions of preferential M1 muscarinic antagonists and cocaine. Dose-dependent increases in extracellular levels of dopamine in selected brain areas, the nucleus accumbens (NAc) shell and core, and the prefrontal cortex, were produced by cocaine but not by the preferential M1 antagonists telenzepine and trihexyphenidyl. When administered with cocaine, however, both M1 antagonists dose-dependently increased the effects of cocaine on dopamine in the NAc shell, and these effects were selective in that they were not obtained in the NAc core or in the prefrontal cortex. Telenzepine also increased locomotor activity, although the effect was small compared with that of cocaine. The locomotor stimulant effects of trihexyphenidyl, in contrast, approached those of cocaine. Telenzepine attenuated, whereas trihexyphenidyl enhanced the locomotor stimulant effects of cocaine, with neither drug facilitating cocaine-induced stereotypy. The present results indicate that preferential antagonist effects at muscarinic M1 receptors do not uniformly alter all of the effects of cocaine, nor do they explain the differences in effects of cocaine and benztropine analogs, and that the alterations in dopamine levels in the NAc shell do not predict the behavioral effects of the interactions with cocaine.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-3565
pubmed:author
pubmed:issnType
Print
pubmed:volume
321
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
334-44
pubmed:meshHeading
pubmed-meshheading:17255465-Animals, pubmed-meshheading:17255465-Benztropine, pubmed-meshheading:17255465-Brain Chemistry, pubmed-meshheading:17255465-Cocaine, pubmed-meshheading:17255465-Dopamine, pubmed-meshheading:17255465-Dopamine Plasma Membrane Transport Proteins, pubmed-meshheading:17255465-Dopamine Uptake Inhibitors, pubmed-meshheading:17255465-Male, pubmed-meshheading:17255465-Microdialysis, pubmed-meshheading:17255465-Motor Activity, pubmed-meshheading:17255465-Muscarinic Antagonists, pubmed-meshheading:17255465-Nucleus Accumbens, pubmed-meshheading:17255465-Prefrontal Cortex, pubmed-meshheading:17255465-Protein Binding, pubmed-meshheading:17255465-Rats, pubmed-meshheading:17255465-Rats, Sprague-Dawley, pubmed-meshheading:17255465-Receptor, Muscarinic M1, pubmed-meshheading:17255465-Stereotyped Behavior, pubmed-meshheading:17255465-Synaptic Transmission
pubmed:year
2007
pubmed:articleTitle
Effects of muscarinic M1 receptor blockade on cocaine-induced elevations of brain dopamine levels and locomotor behavior in rats.
pubmed:affiliation
Psychobiology, Department of Health and Human Services, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. gtanda@intra.nida.nih.gov
pubmed:publicationType
Journal Article, Research Support, N.I.H., Intramural