Effect of naloxone, haloperidol and propranolol on cyclic 3',5'-adenosine monophosphate content of rat amygdala

Eur J Pharmacol. 1979 Dec 20;60(4):345-7. doi: 10.1016/0014-2999(79)90239-5.

Abstract

Naloxone (0.4 mg/kg, i.p.) causes an increase of cyclic adenosine monophosphate levels in the amygdala, but not in the hippocampus, caudate, or hypothalamus, of rats. The effect is antagonized by haloperidol (0.5 mg/kg, i.p.) and by propranolol (0.5 mg/kg, i.p.). This is consistent with the hypothesis of a tonic inhibitory influence of endogenous opiates on central dopaminergic and beta-noradrenergic systems. Haloperidol had an effect of its own on amygdala cyclic adenosine monophosphate levels which was blocked by propranolol. This suggests the possibility of an antagonistic interaction between dopaminergic and beta-noradrenergic innervation on this structure.

MeSH terms

  • Amygdala / drug effects
  • Amygdala / metabolism*
  • Animals
  • Caudate Nucleus / metabolism
  • Cyclic AMP / metabolism*
  • Drug Interactions
  • Female
  • Haloperidol / pharmacology*
  • Hippocampus / metabolism
  • Hypothalamus / metabolism
  • In Vitro Techniques
  • Naloxone / pharmacology*
  • Nerve Tissue Proteins / metabolism
  • Propranolol / pharmacology*
  • Rats

Substances

  • Nerve Tissue Proteins
  • Naloxone
  • Propranolol
  • Cyclic AMP
  • Haloperidol