Anatomy and pharmacology of cocaine priming-induced reinstatement of drug seeking

Cocaine addiction in human addicts is characterized by a high rate of relapse following successful detoxification. Relapse to drug taking/seeking can be precipitated by several stimuli including, but not limited to, re-exposure to cocaine itself. In order to understand the mechanisms underlying coca...

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Bibliographic Details
Published inEuropean journal of pharmacology Vol. 526; no. 1; pp. 65 - 76
Main Authors Schmidt, Heath D., Anderson, Sharon M., Famous, Katie R., Kumaresan, Vidhya, Pierce, R. Christopher
Format Journal Article Conference Proceeding
LanguageEnglish
Published Amsterdam Elsevier B.V 05.12.2005
Elsevier
Subjects
Addiction
Basal Ganglia - physiology
Biological and medical sciences
Cocaine - pharmacology
Cocaine-Related Disorders - etiology
Cocaine-Related Disorders - physiopathology
Dopamine
Dopamine - physiology
Glutamate
Glutamic Acid - physiology
Humans
Limbic System - physiology
Medical sciences
Models, Neurological
Neural Pathways - physiology
Nucleus accumbens
Pharmacology. Drug treatments
Recurrence
Relapse
Synaptic Transmission - drug effects
Nucleus accumbens
Relapse
Dopamine
Addiction
Glutamate
Drug addiction
CNS stimulant
Psychotropic
Central nervous system
Basal ganglion
Catecholamine
Anatomy
Encephalon
Local anesthetic
Ester
Excitatory aminoacid
Neurotransmitter
Cocaine
Drug of abuse
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Summary:Cocaine addiction in human addicts is characterized by a high rate of relapse following successful detoxification. Relapse to drug taking/seeking can be precipitated by several stimuli including, but not limited to, re-exposure to cocaine itself. In order to understand the mechanisms underlying cocaine craving, a substantial effort has been devoted to elucidating the anatomical and neurochemical bases underlying cocaine priming-induced reinstatement, an animal model of relapse. Here, we review evidence that changes in dopaminergic and glutamatergic transmission in limbic/basal ganglia circuits of interconnected nuclei including the medial prefrontal cortex, nucleus accumbens, ventral pallidum, amygdala, hippocampus, orbitofrontal cortex, neostriatum and thalamus underlie cocaine priming-induced reinstatement of cocaine seeking. Maladaptive changes in the processing of motivationally relevant stimuli by these circuits following cocaine self-administration result in drug craving and compulsive drug seeking upon re-exposure to cocaine.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2005.09.068