N-methyl-D-aspartate receptor-independent long-term potentiation in area CA1 of rat hippocampus: input-specific induction and preclusion in a non-tetanized pathway.

We previously reported that an N-methyl-D-aspartate receptor-independent component of long-term potentiation with an apparent delayed onset can be induced in area CA1 of the hippocampus. Here we show that some but not all of this delay in onset can be accounted for by a transient heterosynaptic depression. We also show that N-methyl-D-aspartate receptor-independent long-term potentiation is induced only in the input pathway tetanized, and not in a second pathway. However, prior induction of N-methyl-D-aspartate receptor-independent long-term potentiation in one pathway precludes later induction in an independent pathway. Calcium entry through dihydropyridine-sensitive Ca2+ channels may be a critical step for induction of N-methyl-D-aspartate receptor-independent long-term potentiation in area CA1 [Grover L. M. and Teyler T.J. (1990) Nature 347, 477-479]. Since the distribution [Westenbroek R. E. et al. (1990) Nature 347, 281-284] of dihydropyridine-sensitive Ca2+ channels in CA1 neuron dendrites does not suggest a basis for input-specific induction of long-term potentiation, an additional process may confer the specificity we observed. Tetanic stimulation of afferents into area CA1 can elicit several processes: a transient heterosynaptic depression, and a transient homosynaptic potentiation, as well as N-methyl-D-aspartate receptor-dependent and -independent long-term potentiation.