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Long-term potentiation (LTP) and long-term depression (LTD), two prominent forms of synaptic plasticity at glutamatergic afferents to CA1 hippocampal pyramidal cells, are both triggered by the elevation of postsynaptic intracellular calcium concentration (Ca2+i). To understand how one signaling molecule can be responsible for triggering two opposing forms of synaptic modulation, different postsynaptic Ca2+i elevation patterns were generated by a new caged calcium compound nitrophenyl-ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid in CA1 pyramidal cells. We found that specific patterns of Ca2+i elevation selectively activate LTP or LTD. In particular, only LTP was triggered by a brief increase of Ca2+i with relatively high magnitude, which mimics the Ca2+i rise during electrical stimulation typically used to induce LTP. In contrast, a prolonged modest rise of Ca2+i reliably induced LTD. An important implication of the results is that both the amplitude and the duration of an intracellular chemical signal can carry significant biological information.
Yang et al. (Mon,) studied this question.