|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
1
|
|
pubmed:dateCreated |
2007-9-17
|
|
pubmed:abstractText |
Although escalation of consumption is an important characteristic of cocaine dependence, the neurobiological mechanisms that mediate this phenomenon have not been fully described. In this study, we used male, Sprague-Dawley rats to measure the effects of acute and continuous intracerebroventricular (ICV) administration of the competitive NMDA receptor antagonist, LY235959, on cocaine self-administration behavior under various schedules of reinforcement and access conditions. Single ICV infusions of LY235959 (0.03-0.3 microg/5 microl) produced dose-dependent and statistically significant decreases in the number of cocaine infusions earned under a progressive ratio schedule of reinforcement. In a second experiment, vehicle or LY235959 (0.2-0.3 microg/day) was continuously administered ICV to rats via surgically-implanted subcutaneous osmotic minipump/intracranial cannula assemblies. Both vehicle- and LY235959-treated rats significantly escalated cocaine self-administration over the 10 long access sessions; however, rats treated with LY235959 escalated cocaine self-administration faster and to a greater degree than vehicle-treated rats. There was a statistically significant increase in cocaine infusions earned under the PR schedule in LY235959-treated rats, but not vehicle-treated rats, after 10 long access cocaine self-administration sessions. These data support the hypothesis that escalation of cocaine consumption is mediated by hypo-glutamatergic tone in the central nervous system and this facilitation of escalation is associated with an increase in motivation to respond for cocaine.
|
|
pubmed:grant |
|
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-10871318,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-10942857,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11245826,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11351936,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11408554,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11517248,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11694884,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-11860480,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-12055635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-12459930,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-12614686,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-12778052,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-14625453,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-14647962,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-14712340,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-15650844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-15702135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-16000629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-16024734,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-16772537,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-1834088,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-2671566,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-7606438,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-7714800,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-7870971,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-9121809,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-9765157,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17716714-9826231
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Nov
|
|
pubmed:issn |
0091-3057
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
88
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
82-8
|
|
pubmed:dateRevised |
2010-9-16
|
|
pubmed:meshHeading |
pubmed-meshheading:17716714-Animals,
pubmed-meshheading:17716714-Catheterization, Peripheral,
pubmed-meshheading:17716714-Cocaine,
pubmed-meshheading:17716714-Cocaine-Related Disorders,
pubmed-meshheading:17716714-Conditioning, Operant,
pubmed-meshheading:17716714-Data Interpretation, Statistical,
pubmed-meshheading:17716714-Dose-Response Relationship, Drug,
pubmed-meshheading:17716714-Excitatory Amino Acid Antagonists,
pubmed-meshheading:17716714-Injections, Intraventricular,
pubmed-meshheading:17716714-Isoquinolines,
pubmed-meshheading:17716714-Male,
pubmed-meshheading:17716714-Rats,
pubmed-meshheading:17716714-Rats, Sprague-Dawley,
pubmed-meshheading:17716714-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:17716714-Reinforcement (Psychology),
pubmed-meshheading:17716714-Reinforcement Schedule,
pubmed-meshheading:17716714-Self Administration
|
|
pubmed:year |
2007
|
|
pubmed:articleTitle |
Continuous intracerebroventricular infusion of the competitive NMDA receptor antagonist, LY235959, facilitates escalation of cocaine self-administration and increases break point for cocaine in Sprague-Dawley rats.
|
|
pubmed:affiliation |
Department of Psychology, University of Colorado at Denver and Health Sciences Center, Downtown Denver Campus, CO 80217, United States. richard.allen@cudenver.edu
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|
