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 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.
Schmidt
Heath D
HD
Department of Pharmacology, Boston University School of Medicine, 715 Albany Street, Boston, MA 02118, USA.
Anderson
Sharon M
SM
Famous
Katie R
KR
Kumaresan
Vidhya
V
Pierce
R Christopher
RC
D001479:Basal Ganglia / Q000502:physiology; D003042:Cocaine / Q000494:pharmacology; D019970:Cocaine-Related Disorders / Q000209:etiology / Q000503:physiopathology*; D004298:Dopamine / Q000502:physiology*; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D008032:Limbic System / Q000502:physiology; D008959:Models, Neurological; D009434:Neural Pathways / Q000502:physiology*; D012008:Recurrence; D009435:Synaptic Transmission / Q000187:drug effects
D018698:Glutamic Acid; D003042:Cocaine; D004298:Dopamine