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Increase in cortical endocannabinoid signaling in a rat model of basal forebrain cholinergic dysfunction.

Llorente-Ovejero Alberto, Manuel Iván, Giralt Maria Teresa, Rodríguez-Puertas Rafael

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Abstract

The basal forebrain cholinergic pathways progressively degenerate during the progression of Alzheimer's disease, leading to an irreversible impairment of memory and thinking skills. The stereotaxic lesion with 192IgG-saporin in the rat brain has been used to eliminate basal forebrain cholinergic neurons and is aimed at emulating the cognitive damage described in this disease in order to explore its effects on behavior and on neurotransmission. Learning and memory processes that are controlled by cholinergic neurotransmission are also modulated by the endocannabinoid (eCB) system. The objective of the present study is to evaluate the eCB signaling in relation to the memory impairment induced in adult rats following a specific cholinergic lesion of the basal forebrain. Therefore, CB

MeSH Terms

AnimalsAntibodies, MonoclonalBasal ForebrainCerebral CortexCholinergic NeuronsDisease Models, AnimalEndocannabinoidsGlutamate DecarboxylaseGuanosine 5'-O-(3-Thiotriphosphate)Learning DisabilitiesMaleMemory DisordersNerve Tissue ProteinsRandom AllocationRats, Sprague-DawleyReceptor, Cannabinoid, CB1Receptors, Growth FactorReceptors, Nerve Growth FactorRibosome Inactivating Proteins, Type 1Saporinsgamma-Aminobutyric Acid