Molecular Mechanisms Underlying Aging Associated Decline

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Molecular Mechanisms Underlying Aging Associated Decline in Memory Storage Cognitive function depends on proper wiring and functional connections within neuronal circuits. Despite advances in understanding human aging and aging-associated cognitive decline, molecular and cellular mechanisms underlying aging associated impairments in learning and memory are still poorly understood. In particular, very little is known about whether physiological and molecular changes in identified neurons that are important for learning lead to aging associated decline in long-term memory storage. We approach this problem by delineating the aging associated changes in two well characterized neurons, presynaptic LE sensory neurons (LESNs) and postsynaptic L7 motor neuron (L7MN) of Aplysia whose normal functioning is critical for the learning of gill withdrawal reflex (GWR). Along with us, others have used Aplysia as a model to understand aging associated changes in neuronal physiology, response to neurotransmitters, gene expression and behavioral learning. In a study that examined electrophysiological and gene expression changes in identified neuron R15 of Aplysia, we recently described specific changes in burst firing and action potentials, expression of several genes in R15 during aging and specific changes in the expression of key regulators of transcription and translation in four identified neurons (L7, L11, R2, R15) of Aplysia. The long-term goal of this project is to identify synaptic

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