Uncompetitive inhibition of [3H]1,3-di-o-tolyl-guanidine-defined sigma binding sites by desipramine, propranolol and alprenolol in rat brain

Eur J Pharmacol. 1997 Jul 23;331(2-3):319-23. doi: 10.1016/s0014-2999(97)01051-0.

Abstract

Desipramine, imipramine, clomipramine, (-)-propranolol, (-)-alprenolol, (+/-)-pentazocine and risperidone caused a concentration-dependent inhibition of 6 nM [3H]DTG (1,3-di-o-tolylguanidine)-defined sigma (sigma) binding with Ki values of about 0.5-2.5 microM in well-washed homogenates obtained from rat cerebral cortex. The saturation studies revealed that the inhibition by desipramine (1-4 microM), (-)-propranolol (1 microM) and (-)-alprenolol (3 microM) resulted from a reduction of the Bmax value without alteration of the Kd of [3H]DTG binding to the cortex or hippocampus. In contrast, imipramine, (+/-)-pentazocine, clomipramine and risperidone competitively attenuated the cortical or hippocampal [3H]DTG binding. These findings demonstrate the uncompetitive inhibition of [3H]DTG binding by neuroactive drugs, thereby providing further support for the possible multiple regulation of cerebral sigma receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Antagonists / pharmacology*
  • Alprenolol / pharmacology*
  • Animals
  • Antidepressive Agents, Tricyclic / pharmacology*
  • Desipramine / pharmacology*
  • Guanidines / pharmacology*
  • Kinetics
  • Male
  • Propranolol / pharmacology*
  • Rats
  • Rats, Wistar
  • Receptors, sigma / antagonists & inhibitors*
  • Receptors, sigma / metabolism

Substances

  • Adrenergic beta-Antagonists
  • Antidepressive Agents, Tricyclic
  • Guanidines
  • Receptors, sigma
  • Alprenolol
  • Propranolol
  • 1,3-ditolylguanidine
  • Desipramine