Biochemical and behavioral evidence for an interaction between ethanol and calcium channel antagonists

J Neural Transm. 1988;74(3):181-93. doi: 10.1007/BF01244784.

Abstract

In the present series of experiments we have studied the effects of the dihydropyridine calcium channel antagonist nifedipine on ethanol-induced changes in behavior and dopamine (DA) release and metabolism. The locomotor-stimulatory effect of low doses of ethanol (2.5 g/kg) was antagonized by nifedipine, whereas ethanol-induced sedation observed after higher doses (4.5 g/kg) was potentiated. Biochemical studies indicated that ethanol enhanced the metabolism and release of DA in the striatum and the DA-rich limbic regions measured by post mortem analyses of DA-metabolites by HPLC with electrochemical detection and by in vivo voltammetry in anaesthetized rats, respectively. Pretreatment with nifedipine antagonized the stimulatory effects of ethanol on the DA-system. Nifedipine reduced the preference for ethanol, estimated by the relative intake of ethanol (6% v/v) and water in a free-choice situation, suggesting an influence of nifedipine not only on the stimulatory but also on the positive reinforcing effects of ethanol. The present results suggest that the locomotor-stimulatory and positive reinforcing effects of ethanol as well as its enhancing effect on dopaminergic activity may involve an enhancement of calcium mediated mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium Channel Blockers / pharmacology*
  • Dopamine / metabolism*
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Ethanol / pharmacology*
  • Female
  • Male
  • Mice
  • Motor Activity / drug effects*
  • Nifedipine / pharmacology*
  • Rats
  • Rats, Inbred Strains
  • Time Factors

Substances

  • Calcium Channel Blockers
  • Ethanol
  • Nifedipine
  • Dopamine