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Beinfeld 2001

Beinfeld 2001

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Neuroscience Letters 301 (2001) 69±71 
Activation of CB1 cannabinoid receptors in rat hippocampalslices inhibits potassium-evoked cholecystokinin release,a possible mechanism contributing to the spatial memorydefects produced by cannabinoids
Margery C. Beinfeld*, Kelly Connolly
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 136 HarrisonAvenue,Boston, MA 02111, USAReceived 10 November 2000; received in revised form 15 December 2000; accepted 27 December 2000AbstractCannabinoid use is known to disrupt learning and memory in a number of species. cholecystokinin (CCK) release andCCK receptors have been implicated in spatial memory processes in rodents. Rat hippocampal CCK interneuronsexpresscannabinoid 1 receptors (CB1). The CB1 agonist R(1)WIN 55,212±2 (WIN1), at 1 and 10 mmol, strongly inhibitedpotas-sium-evoked CCK release from rat hippocampal slices, while theinactive isomer S(2)WIN,55,212±3 (WIN2) had noeffect.CCKreleasefrom cerebral corticalsliceswasnot altered byWIN1.q 2001Elsevier ScienceIreland Ltd.Allrights reserved.Keywords: Cholecystokinin; CB1; Cannabinoids; Spatial memory; WIN 55,212±2
Cannabinoids have been consumed for a long time for medical and recreational uses. They are known to causeeuphoria, reduce anxiety, reduce pain, impair spatialmemory and increase appetite [6]. An endogenous cannabi-noid neurotransmitter or neuromodulator system consistingof two cannabinoid receptors and the endogenous ligands,anandamide (N-arachidonylethanolamine) and 2-arachido-nylglycerol has been identi®ed. CB1 and its splice variantCB1A are found predominantly in the brain, being veryabundant in hippocampus, cerebellum and striatum. CB2is present mainly in the periphery. Cannabinoids inhibitadenylate cyclase activity and reduce cholinergic, glutama-tergic, gamino butyric acid (GABA)ergic and dopaminergicneurotransmission [1].Cholecystokinin (CCK) is one of the most abundantpeptides in the cortex and hippocampus [3]. CCK-positiveinterneurons in the rodent hippocampus contain GABA [9]and at least 86% of CB1 positive interneurons in the hippo-campus express CCK, this represents 97% of all CCK-posi-tive interneurons. Co-localization of CCK and CB1receptors has been con®rmed by two other groups [11,16].The synthetic cannabinoid agonist WIN 55,212±2 (WIN1)decreased electrical ®eld stimulation-induced
H GABArelease from superfused rat hippocampal slices [10].Activation of CB1 receptors may cause desynchroniza-tion of principal cells and disrupt theta rhythms resulting indisruption of spatial memory. In rodents, cannabinoids areknown to inhibit LTP and to inhibit short-term and spatial

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