Postcocaine depression and sensitization of brain-stimulation reward: Analysis of reinforcement and performance effects

https://doi.org/10.1016/0091-3057(90)90242-AGet rights and content

Abstract

The effects of acute and chronic cocaine administration on intracranial self-stimulation (ICSS) were evaluated in a two-hole nose-poke discrimination paradigm. Analysis of ICSS rates as a function of current intensity revealed that cocaine increased rates of responding in a dose-dependent manner (5.0–20.0 mg/kg), resulted in a shift to the left of the rate-intensity function, and decreased thresholds for half-maximal responding. Brain-stimulation reward was modified by chronic exposure to cocaine, however, the direction of change was dependent on the schedule of drug administration. Repeated daily administration of cocaine (40.0 mg/kg) and ICSS testing 24 hr postinjection decreased rates and increased reward thresholds. A response depression was also observed when time-dependent variations in ICSS performance were evaluated after repeated cocaine administration. Using a different chronic cocaine/test schedule (30.0 mg/kg, twice daily), a sensitization of ICSS and decreased reward thresholds developed when rate-intensity functions were determined after 5-day drug intervals. These findings were discussed in terms of the role of dopamine in modulating central reward processes. It was suggested that depressed reward-system functioning might reflect reduced dopamine synthesis following cocaine withdrawal, and the ICSS sensitization was related to long-term compensatory changes in dopamine neurotransmission possibly involving presynaptic mechanisms.

References (53)

  • L. Hernandez et al.

    Food reward and cocaine increase extracellular dopamine in the nucleus accumbens as measured by microdialysis

    Life Sci.

    (1988)
  • M.S. Kleven et al.

    Lack of long-term monoamine depletions following repeated or continuous exposure to cocaine

    Brain Res. Bull.

    (1988)
  • L. Kokkinidis et al.

    Enhanced self-stimulation responding from the substantia nigra after chronic amphetamine treatment: A role for conditioning factors

    Pharmacol. Biochem. Behav.

    (1980)
  • L. Kokkinidis et al.

    Post-amphetamine depression of self-stimulation responding from the substantia nigra: Reversal by tricyclic antidepressants

    Pharmacol. Biochem. Behav.

    (1980)
  • J.M. Liebman

    Discriminating between reward and performance: A critical review of intracranial self-stimulation methodology

    Neurosci. Biobehav. Rev.

    (1983)
  • B.D. McCarter et al.

    The effects of long-term administration of antidepressant drugs on intracranial self stimulation responding in rats

    Pharmacol. Biochem. Behav.

    (1988)
  • E. Miliaressis et al.

    The curve-shift paradigm in self-stimulation

    Physiol. Behav.

    (1986)
  • A.G. Phillips et al.

    Neurochemical correlates of brain-stimulation reward measured by ex vivo and in vivo analyses

    Neurosci. Biobehav. Rev.

    (1989)
  • P.A. Predy et al.

    Sensitization to the effects of repeated amphetamine administration on intracranial self-stimulation: evidence for changes in reward processes

    Behav. Brain Res.

    (1984)
  • M.E.A. Reith et al.

    Structural requirements for cocaine congeners to interact with dopamine and serotonin uptake sites in mouse brain and to induce stereotyped behavior

    Biochem. Pharmacol.

    (1986)
  • D.C. Roberts et al.

    On the role of ascending catecholaminergic systems in intravenous self-administration of cocaine

    Pharmacol. Biochem. Behav.

    (1977)
  • T.E. Robinson et al.

    Behavioral sensitization is accompanied by an enhancement in amphetamine-stimulated dopamine release from striatal tissue in vitro

    Eur. J. Pharmacol.

    (1982)
  • T.E. Robinson et al.

    Enduring changes in brain and behavior produced by chronic amphetamine administration: a review and evaluation of animal models of amphetamine psychosis

    Brain Res. Rev.

    (1986)
  • T.E. Robinson et al.

    Persistent sensitization of dopamine neurotransmission in ventral striatum (nucleus accumbens) produced by prior experience with (+)-amphetamine: a microdialysis study in freely moving rats

    Brain Res.

    (1988)
  • M.A. Sherer

    Intravenous cocaine: psychiatric effects, biological mechanisms

    Biol. Psychiatry

    (1988)
  • M.E. Trulson et al.

    Chronic cocaine administration depletes tyrosine hydroxylase immunoreactivity in rat brain nigral striatal system: quantitative light microscopic studies

    Exp. Neurol.

    (1986)
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