6533b83afe1ef96bd12a709a

RESEARCH PRODUCT

Inhibition by Anandamide and Synthetic Cannabimimetics of the Release of [3H]d-Aspartate and [3H]GABA from Synaptosomes Isolated from the Rat Hippocampus

Paolo PreziosiMaria MartireMonia D'amicoCarla Cannizzaro

subject

MaleCannabinoid receptorSettore BIO/14 - FARMACOLOGIAPolyunsaturated Alkamidesmedicine.medical_treatmentHippocampusArachidonic AcidsPharmacologyHippocampal formationDepolarization-induced suppression of inhibitionHippocampusBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundglutamate releasemedicineAnimalsRats WistarCannabinoidgamma-Aminobutyric AcidCannabinoid Receptor AgonistsAspartic AcidCannabinoidsChemistryGeneral MedicineAnandamideCyclohexanolsgaba releaseEndocannabinoid systemRatsKineticsnervous systemBiochemistryAnimals Arachidonic Acids Aspartic Acid Calcium Cannabinoids Capsaicin Cyclohexanols gamma-Aminobutyric Acid Hippocampus Kinetics Polyunsaturated Alkamides Potassium Rats Receptors Cannabinoid SynaptosomesPotassiumCalciumlipids (amino acids peptides and proteins)CannabinoidCapsaicinCapsazepineEndocannabinoidsSynaptosomes

description

Cannabinoids (CB) can act as retrograde synaptic mediators of depolarization-induced suppression of inhibition or excitation in hippocampus. This mechanism may underlie the impairment of some cognitive processes produced by these compounds, including short-term memory formation in the hippocampus. In this study, we investigated several compounds known to interact with CB receptors, evaluating their effects on K +-evoked release of [ 3H]d-aspartate ([ 3H]d-ASP) and [ 3H]GABA from superfused synaptosomes isolated from the rat hippocampus. [ 3H]d-ASP and [ 3H]GABA release were inhibited to different degrees by the synthetic cannabinoids WIN 55,212-2; CP 55,940, and arachidonyl-2′- chloroethylamide/N-(2-chloroethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide (ACEA), as well as by the endocannabinoids, anandamide (AEA), and 2-arachidonoylglycerol (2-AG). Both types of release were also inhibited by capsaicin. The inhibition produced by each of the cannabinoid compounds and capsaicin was unaffected by capsazepine or by the CB1-receptor antagonists AM-251 and SR141716A. The mechanism underlying AEA- and synthetic CB-induced inhibition of the release of [ 3H]GABA and [ 3H]d-ASP from rat hippocampal synaptosomes might not involve activation of presynaptic CB1 receptors.

yearjournalcountryeditionlanguage
2004-01-01Neurochemical Research
https://doi.org/10.1023/b:nere.0000029569.20266.3f