Linked Life Data

18155756

Source:http://linkedlifedata.com/resource/pubmed/id/18155756

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2008-1-18
pubmed:abstractText
Cocaine-induced increases in dopamine (DA) contribute importantly to cocaine effects on behavior but, the role of concomitant increases in norepinephrine (NE) and serotonin (5-HT) is less well understood. In order to selectively block the increases in NE and 5-HT evoked by cocaine, autoreceptor preferring low doses (0.01, 0.025 and 0.05 mg/kg) of the a2 agonist, Clonidine or the 5-HT1A agonist, 8-OHDPAT were given as pretreatments 20 min prior to saline or cocaine (10.0 mg/kg) in separate groups of rats (N=10). With pharmacological stimulation of NE and 5-HT autoreceptors, release of these neurotransmitters would be suppressed and, therefore, less available for re-uptake blockade by cocaine. With increasing dose levels, Clonidine had marked inhibitory effects on spontaneous and cocaine-induced locomotion, grooming and rearing. 8-OHDPAT pretreatment also suppressed spontaneous locomotion, grooming and rearing; but, in contrast, did not reduce the cocaine locomotor stimulant effects. 8-OHDPAT, however, did suppress central zone entry and rearing in cocaine treated rats. Using ex vivo methods, we found that 8-OHDPAT selectively reduced 5-HT metabolism in the medial frontal cortex (MFC) and subcortical limbic brain. Clonidine selectively reduced NE metabolism in the MFC, but decreased both DA and 5-HT metabolism in the subcortical limbic brain without affecting NE metabolism. This diverse and broad spectrum of Clonidine effects upon neurotransmitters and behavior is striking and points-up the important, complex and integrative role of NE in brain function. While both Clonidine and 8-OHDPAT can substantially attenuate a number of cocaine behavioral effects, these inhibitory effects appear to be secondary to reductions in the behavioral baseline rather than reversals of cocaine effects.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0091-3057
pubmed:author
pubmed:issnType
Print
pubmed:volume
89
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
54-63
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:18155756-8-Hydroxy-2-(di-n-propylamino)tetralin, pubmed-meshheading:18155756-Adrenergic Agonists, pubmed-meshheading:18155756-Adrenergic alpha-Agonists, pubmed-meshheading:18155756-Animals, pubmed-meshheading:18155756-Clonidine, pubmed-meshheading:18155756-Cocaine, pubmed-meshheading:18155756-Dopamine Uptake Inhibitors, pubmed-meshheading:18155756-Limbic System, pubmed-meshheading:18155756-Male, pubmed-meshheading:18155756-Norepinephrine, pubmed-meshheading:18155756-Prefrontal Cortex, pubmed-meshheading:18155756-Rats, pubmed-meshheading:18155756-Rats, Sprague-Dawley, pubmed-meshheading:18155756-Receptor, Serotonin, 5-HT1A, pubmed-meshheading:18155756-Serotonin, pubmed-meshheading:18155756-Serotonin Receptor Agonists, pubmed-meshheading:18155756-Sympathetic Nervous System
pubmed:year
2008
pubmed:articleTitle
Effects on spontaneous and cocaine-induced behavior of pharmacological inhibition of noradrenergic and serotonergic systems.
pubmed:affiliation
Research and Development Service 151, VA Medical Center, Syracuse, NY 13210, USA. careyr@cnyrc.org
pubmed:publicationType
Journal Article