Evaluation of the nicotinic cholinergic neuroplasticity at the amygdala, after cognitive stimulation, in an animal model of neurodegeneration and in aging

Abstract

Cognitive processes depend on relationship among cortex, hyppocampus and other limbic structures. Chronic degeneration of these structures leads to progressive dementia with decline in memory, as happens in Alzheimer's disease. Recent results from our group showed that the infusion of amyloid-beta peptide (A-beta) in the lateral ventricle of rats, followed by frequent stimulus at the active avoidance apparatus, promoted cortical and hyppocampal neurodegeneration and partial reduction of memory. These animals also presented an increase in density of acetylcholine (ACh) binding sites on alpha7 nicotinic receptors in brain regions related to emotions and defense responses, like the amygdala. Our hypothesis concerns the stimulation of new neuronal pathways which contributed to memory maintenance. This study will analyze the cholinergic neuroplasticity in the amydala and its contribution to memory processes when that is degeneration in cortex and hippocampus. For this purpose, we will use active avoidance and inhibitory avoidance apparatus to investigate learning and memory, enriched environment as a non-stressing cognitive stimulus, autoradiography for alpha7 nicotinic receptors and immunohistochemistry to evaluate formation of ACh and neuroplasticity. We will use transgenic mice for the Alzheimer's disease and rats with different ages. This study can be the base for new therapeutic approaches for neuropsychiatric disturbs. (AU)