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Hampson 98, memory storage, Neurobiol Disease.pdf

Hampson 98, memory storage, Neurobiol Disease.pdf

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Published by: Matias Ceballos Guzman on Dec 09, 2010
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 Neurobiology of Disease 5, 474–482 (1998)Article No. NB980223
Role of Cannabinoid Receptors in Memory Storage
Robert E. Hampson and SamA. Deadwyler 
 Department of Physiology & Pharmacology and Center for the Neurobiological  Investigation of Drug Abuse, Wake Forest University School of Medicine,Winston–Salem, North Carolina 27157-1083
Studies have shown that 9-tetrahydrocannabinol, the principal psychoactive ingredient in marijuana, produces memory deficits similar to those produced by neurochemical lesions of the hippocampus.Such lesions impair performance in short-term spatial memory tasks learned prior to the lesion.Animals trained in the behavioral task following the lesion can still perform the task, but learn adifferent behavioral strategy. Cannabinoid agonists impair behavioral performance in a delay-dependent manner similar to that produced by lesions, but also shift the behavioral response strategy.A possible role for cannabinoid receptors and endogenous cannabinoids may thus be to regulate thestorage (i.e., encoding) of information, aswell as themeans bywhichthat information is retrieved.1998Academic Press
The role of cannabinoids in memory processes can be traced to early observations in humans that signifi-cant disruption of short-term recall of events was themost consistent disruptive effect in experimental testsof marijuana intoxication (1). More recent investiga-tions have confirmed that the memory disruptiveeffect of 
-tetrahydrocannabinol (THC) in humans isalso accompanied by several other perceptual anddisorientation effects (2,3). Early studies on the effectsof high concentrations of 
-THC (i.e., 10 mg/kg) inrodents showed profoundly impaired maze learningand operant behavior during and after chronic THCexposure (4–6). Initial studies of low doses of 
-THCon hippocampal memory processes showed subtle butconsistent dose-dependent impairment (7,8). In subse-quent years the laboratory has compiled considerabledata on the nature of these effects in many different behavioral paradigms. The major overriding finding isthat effects on hippocampal-mediated processes areconsistent with respect to dose range and severity of disruption (9). One of the most intriguing findings inthis regard has been the observation that cannabinoidsdisrupt processing of sensory information within hip- pocampal circuits (10,11). This disruption occurs pri-marily in the dentate gyrus, where high densities of cannabinoid receptors exist (12,13). Local applicationof the potent cannabinoid agonist CP55,940 to thehippocampus of rats has shown that the memoryimpairment produced by cannabinoids can be sepa-
rated from collateral motor effects. Intrahippocampalinjection of CP55,940 produced a dose-dependent im- pairment of maze performance, with no change in thetime to complete the task (14). Application of the

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