The Neurobiology of Cocaine-Induced Reinforcement

  1. Gregory R. Bock Organizer and
  2. Julie Whelan
  1. H. C. Fibiger1,
  2. A. G. Phillips2 and
  3. E. E. Brown1

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514245.ch7

Ciba Foundation Symposium 166 - Cocaine: Scientific and Social Dimensions

Ciba Foundation Symposium 166 - Cocaine: Scientific and Social Dimensions

How to Cite

Fibiger, H. C., Phillips, A. G. and Brown, E. E. (2007) The Neurobiology of Cocaine-Induced Reinforcement, in Ciba Foundation Symposium 166 - Cocaine: Scientific and Social Dimensions (eds G. R. Bock and J. Whelan), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514245.ch7

Author Information

  1. 1

    Division of Neurological Sciences, Department of Psychiatry, University of British Columbia, 2255 Westbrook Mall, Vancouver BC, Canada V6T 123

  2. 2

    Department of Psychology, University of British Columbia, Vancouver, BC, Canada, V6T 1Z3

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471931799

Online ISBN: 9780470514245

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Keywords:

  • cocaine-induced reinforcement;
  • neurobiology;
  • dopaminergic terminals;
  • neuroleptics;
  • lesion studies

Summary

Cocaine has potent pharmacological actions on a number of monoaminergic systems in the brain, including those that use noradrenaline, dopamine and serotonin as neurotransmitters. There is growing evidence that cocaine's effects on dopaminergic neurons, particularly those that make up the mesolimbic system, are closely associated with its rewarding properties. For example, low doses of doparnine receptor antagonists reliably influence cocaine self-administration, whereas noradrenaline and serotonin receptor antagonists are without consistent effects. Similarly, selective lesions of dopaminergic terminals in the nucleus accumbens, a major target of the mesolimbic dopamine projection, disrupt cocaine self-administration in a manner that is consistent with loss of cocaine-induced reward. The introduction of in vivo brain microdialysis as a tool with which to investigate the neurochemical correlates of motivated behaviour has provided new opportunities for investigating the role of dopamine in the nucleus accumbens in the acquisition and maintenance of cocaine self-administration. Although the body of literature that has been generated by this approach appears to contain some important inconsistencies, these probably reflect the use of inappropriate microdialysis conditions by some investigators. A critical review of the literature suggests that microdialysis results are generally consistent with a role for mesolimbic dopamine in cocaine-induced reward, although it does not seem to be the case that animals will work to maintain consistent increases in extracellular concentrations of dopamine in the nucleus accumbens in all experimental conditions. Elucidation of the complete neural circuitry of cocaine-induced reward remains an important priority for future research.