Chronic cocaine administration alters corticotropin-releasing factor receptors in the rat brain

Brain Res. 1990 Oct 29;531(1-2):322-8. doi: 10.1016/0006-8993(90)90794-c.

Abstract

Two groups of 12 rats received daily injections of cocaine (20 mg/kg, i.p.) or saline for 15 days following bilateral infusions of 6-hydroxydopamine or vehicle into the lateral ventricles. Cocaine administration resulted in significant decreases in CRF receptor labeling primarily in brain areas associated with the mesolimbic/mesocortical dopaminergic system. All of the cocaine-induced changes in CRF binding were attenuated in the lesioned animals, suggesting that these effects may be mediated, in part, through the actions of the drug on dopaminergic neuronal activity. Dopamine may also be involved in the release of CRF in the rat brain since the purported loss of dopaminergic innervations resulted in increased CRF binding in the saline-treated animals.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Autoradiography
  • Brain / drug effects
  • Brain / metabolism*
  • Cerebral Ventricles / drug effects
  • Cerebral Ventricles / physiology
  • Cocaine / toxicity*
  • Corticotropin-Releasing Hormone / metabolism*
  • Desipramine / pharmacology
  • Hydroxydopamines / pharmacology
  • Male
  • Mazindol / metabolism
  • Organ Specificity
  • Oxidopamine
  • Rats
  • Rats, Inbred F344
  • Receptors, Corticotropin-Releasing Hormone
  • Receptors, Neurotransmitter / drug effects
  • Receptors, Neurotransmitter / metabolism*
  • Reference Values
  • Substance-Related Disorders / metabolism*
  • Tritium

Substances

  • Hydroxydopamines
  • Receptors, Corticotropin-Releasing Hormone
  • Receptors, Neurotransmitter
  • Tritium
  • Oxidopamine
  • Corticotropin-Releasing Hormone
  • Mazindol
  • Cocaine
  • Desipramine