Abstract

Abstract In neuronal circuits, excitatory synaptic transmission predominantly occurs at postsynaptic protrusions called dendritic spines. Spines are highly plastic structures capable of formation, enlargement, shrinkage, and elimination over time. Individual spine morphology is widely variable, and evidence suggests these differences in morphology are relevant to spine function. Recent reports provide evidence that spine structural plasticity underlies functional synaptic changes, including those seen in animal models of learning and memory plasticity. Conversely, impairments in cognitive functions, such as those commonly seen in aging, have recently been linked to and correlated with alterations in spine density and morphology. In addition, dendritic spine density and morphology also appear to be altered in various transgenic animal models of neurodegenerative diseases. Ultimately, an understanding of the synaptic basis of age- and disease-related cognitive impairments may lead to the development of drug treatments that can restore or protect synaptic profiles in neural circuits that mediate cognition.

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