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

Eur J Pharmacol. 2005 Dec 5;526(1-3):65-76. doi: 10.1016/j.ejphar.2005.09.068.


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.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Basal Ganglia / physiology
  • Cocaine / pharmacology
  • Cocaine-Related Disorders / etiology
  • Cocaine-Related Disorders / physiopathology*
  • Dopamine / physiology*
  • Glutamic Acid / physiology
  • Humans
  • Limbic System / physiology
  • Models, Neurological
  • Neural Pathways / physiology*
  • Recurrence
  • Synaptic Transmission / drug effects


  • Glutamic Acid
  • Cocaine
  • Dopamine