Abstract
Long-term potentiation (LTP) is an extensively studied model of synaptic plasticity, in part because it is a plausible biological correlate for the Hebbian synaptic modification that forms the basis for theoretical models of neural development, learning, and memory. Although these models must incorporate algorithms that constrain synaptic weight changes, physiological evidence for such mechanisms is limited. Examination of LTP in area CA1 of the hippocampus revealed that the threshold for LTP induction was not fixed but could be strongly influenced by the recent history of synaptic activity. This effect was transient, synapse-specific, and dependent on postsynaptic N-methyl-D-aspartate (NMDA) receptor activation. These results suggest that the threshold for LTP induction may be continually adjusted according to the recent history of NMDA receptor activation and provide a physiological mechanism by which LTP can be transiently inhibited.
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