Synapse specificity of long-term potentiation breaks down with aging.
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.
Ris
Laurence
L
Laboratory of Neurosciences, University of Mons-Hainaut, 7000 Mons, Belgium.
Godaux
Emile
E
D000344:Afferent Pathways / Q000502:physiology; D000375:Aging / Q000378:metabolism / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D020746:Calcium Channels, L-Type / Q000378:metabolism; D004558:Electric Stimulation; D006624:Hippocampus / Q000502:physiology; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000502:physiology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009412:Nerve Fibers / Q000502:physiology; D013569:Synapses / Q000502:physiology*
D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D002118:Calcium