Abstract
We have used low magnesium concentrations and the specific antagonist D-2-amino-5-phosphonopentanoate (D-AP5) to estimate the effects of long-term potentiation (LTP) on the N-methyl-D-aspartate (NMDA) and non-NMDA receptor-mediated components of postsynaptic responses. LTP induction resulted in a considerably larger potentiation of non-NMDA as opposed to NMDA receptor-related currents. Increasing the size of postsynaptic potentials with greater stimulation currents or with paired-pulse facilitation produced opposite effects; i.e., those aspects of the response dependent on NMDA receptors increased to a greater degree than did those components mediated by non-NMDA receptors. These results pose new constraints on hypotheses about the locus and nature of LTP and strongly suggest that postsynaptic modifications are part of the effect.
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Selected References
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