Synapse specificity of long-term potentiation breaks down with aging
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Updated: Jul 16, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
1Laboratory of Neurosciences, University of Mons-Hainaut, 7000 Mons, Belgium.
Abstract:
Memory shows age-related decline. According to the current prevailing theoretical model, encoding of memories relies on modifications in the strength of the synapses connecting the different cells within a neuronal network. The selective increases in synaptic weight are thought to be biologically implemented by long-term potentiation (LTP). Here, we report that tetanic stimulation of afferent fibers in slices from 12-mo-old mice triggers an LTP not restricted to the activated synapses. This phenomenon, which can be anticipated to hinder memory encoding, is suppressed by blocking either L-type Ca(++) channels or Ca(++)-induced Ca(++) release, both well known to become disregulated with aging.
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