Activation of CB1 cannabinoid receptors in rat hippocampal slices inhibits potassium-evoked cholecystokinin release, a possible mechanism contributing to the spatial memory defects produced by cannabinoids

Neurosci Lett. 2001 Mar 23;301(1):69-71. doi: 10.1016/s0304-3940(01)01591-9.

Abstract

Cannabinoid use is known to disrupt learning and memory in a number of species. cholecystokinin (CCK) release and CCK receptors have been implicated in spatial memory processes in rodents. Rat hippocampal CCK interneurons express cannabinoid 1 receptors (CB1). The CB1 agonist R(+)WIN 55,212-2 (WIN+), at 1 and 10 micromol, strongly inhibited potassium-evoked CCK release from rat hippocampal slices, while the inactive isomer S(-)WIN,55,212-3 (WIN-) had no effect. CCK release from cerebral cortical slices was not altered by WIN+.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Benzoxazines
  • Calcium Channel Blockers / pharmacology*
  • Cannabinoids / pharmacology*
  • Cholecystokinin / drug effects*
  • Cholecystokinin / metabolism
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Male
  • Memory / drug effects
  • Memory / physiology
  • Morpholines / pharmacology*
  • Naphthalenes / pharmacology*
  • Potassium Chloride / pharmacology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Cannabinoid
  • Receptors, Drug / drug effects*
  • Receptors, Drug / metabolism

Substances

  • Benzoxazines
  • Calcium Channel Blockers
  • Cannabinoids
  • Morpholines
  • Naphthalenes
  • Receptors, Cannabinoid
  • Receptors, Drug
  • (3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanone
  • Potassium Chloride
  • Cholecystokinin