The discriminative stimulus properties of cocaine

effects of BAY K 8644 and nimodipine

Patrick M. Callahan, Kathryn Cunningham

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Calcium channel blockers appear to reduce the cardiac toxicity of cocaine and some stimulant-induced behaviors. The present experiment was designed to test whether the internal state induced by cocaine is altered by the calcium antagonist nimodipine. Substitution tests with the calcium agonist BAY K 8644 were also conducted in rats (N = 8) trained to discriminate cocaine (10 mg/kg) from saline in a two-lever, water-reinforced drug discrimination paradigm. Cocaine (0.625-10 mg/kg) produced a dose-related increase in drug-lever responding while BAY K 8644 (0.25-2 mg/kg) and nimodipine (0.2-0.8 mg/kg) engendered primarily saline responding. In combination with cocaine (2.5-10 mg/kg), nimodipine shifted the cocaine dose-response curve to the right at doses of 0.2 and 0.4 mg/kg; this attenuation did not increase with higher doses of nimodipine (0.8 and 1.6 mg/kg). The present results suggest that nimodipine may partially block the discriminative stimulus properties of cocaine, however, this reduction is neither robust nor dose-related. Thus, nimodipine might be expected to only marginally alter the subjective cocaine state in humans.

Original languageEnglish (US)
Pages (from-to)143-147
Number of pages5
JournalEuropean Journal of Pharmacology
Volume186
Issue number1
DOIs
StatePublished - Sep 4 1990

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Nimodipine
Cocaine
Calcium
Calcium Channel Blockers
Pharmaceutical Preparations
Water

Keywords

  • (rat)
  • Behaviour
  • Ca channel antagonists
  • Cocaine
  • Drug discrimination
  • Nimodipine

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

Cite this

The discriminative stimulus properties of cocaine : effects of BAY K 8644 and nimodipine. / Callahan, Patrick M.; Cunningham, Kathryn.

In: European Journal of Pharmacology, Vol. 186, No. 1, 04.09.1990, p. 143-147.

Research output: Contribution to journalArticle

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