Linked Life Data

15175391

Source:http://linkedlifedata.com/resource/pubmed/id/15175391

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
22
pubmed:dateCreated
2004-6-3
pubmed:abstractText
Stimulant drugs of abuse have several effects on neural activity, including altering the excitability of dopamine neurons via the noradrenergic and glutamatergic systems. Thus, an interaction between noradrenergic and glutamatergic systems may play a role in drug-seeking behavior. Although many of the direct pharmacological effects of psychostimulants on dopamine neuron physiology are well established, the neurophysiological bases of drug-seeking behavior have yet to be fully elucidated. The present study measured short-term (3 d) and long-term (14 d) access to cocaine, by self-administration or passive exposure, and the regulation of metabotropic glutamate receptor (mGluR)-mediated inhibition of dopamine cells in rat midbrain slices. The results indicated that alpha-adrenoreceptor modulation of the mGluR-mediated inhibition is selectively reduced in animals that self-administered cocaine for 3 d. This effect was not observed in slices from either yoked cocaine animals, which were given cocaine in an amount and pattern equal to that used for the self-administering animals, or saline control animals. However, after 14 d of cocaine, alpha-adrenoreceptor regulation of the mGluR-mediated inhibition was equally reduced in both self-administering and yoked cocaine animals relative to saline controls. The results suggest that alpha-adrenoreceptor regulation of the mGluR-mediated inhibition is an adaptive cellular mechanism involved in early cocaine self-administration that is distinct from a direct pharmacological effect of cocaine on dopamine neurons. The noradrenergic system could therefore serve to alter the reward value of stimuli that have significant effects on dopamine neuron firing pattern through mGluRs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1529-2401
pubmed:author
pubmed:issnType
Electronic
pubmed:day
2
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5209-15
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15175391-Adrenergic alpha-Agonists, pubmed-meshheading:15175391-Animals, pubmed-meshheading:15175391-Cocaine, pubmed-meshheading:15175391-Cocaine-Related Disorders, pubmed-meshheading:15175391-Conditioning, Operant, pubmed-meshheading:15175391-Dopamine, pubmed-meshheading:15175391-Excitatory Amino Acid Agonists, pubmed-meshheading:15175391-Male, pubmed-meshheading:15175391-Mesencephalon, pubmed-meshheading:15175391-Neural Inhibition, pubmed-meshheading:15175391-Neurons, pubmed-meshheading:15175391-Norepinephrine, pubmed-meshheading:15175391-Patch-Clamp Techniques, pubmed-meshheading:15175391-Phenylephrine, pubmed-meshheading:15175391-Rats, pubmed-meshheading:15175391-Rats, Sprague-Dawley, pubmed-meshheading:15175391-Receptors, Metabotropic Glutamate, pubmed-meshheading:15175391-Self Administration, pubmed-meshheading:15175391-Street Drugs, pubmed-meshheading:15175391-Time Factors
pubmed:year
2004
pubmed:articleTitle
Cocaine self-administration selectively decreases noradrenergic regulation of metabotropic glutamate receptor-mediated inhibition in dopamine neurons.
pubmed:affiliation
The Vollum Institute and Department of Behavioral Neuroscience, Oregon Health and Science University, Portland, Oregon 97201, USA. paladini@ohsu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't