guanosine-5--o-(3-thiotriphosphate) and Learning-Disabilities

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

Topics: Animals; Antibodies, Monoclonal; Basal Forebrain; Cerebral Cortex; Cholinergic Neurons; Disease Models, Animal; Endocannabinoids; gamma-Aminobutyric Acid; Glutamate Decarboxylase; Guanosine 5'-O-(3-Thiotriphosphate); Learning Disabilities; Male; Memory Disorders; Nerve Tissue Proteins; Random Allocation; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Receptors, Growth Factor; Receptors, Nerve Growth Factor; Ribosome Inactivating Proteins, Type 1; Saporins