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 intrac
ellular calcium concentration ([Ca2+](i)). To understand how one signaling
molecule can be responsible for triggering two opposing forms of synaptic m
odulation, different postsynaptic [Ca2+](i) elevation patterns were generat
ed by a new caged calcium compound nitrophenyl-ethylene glycol-bis(beta-ami
noethyl ether)-N,N,N',N'-tetraacetic acid in CA1 pyramidal cells. We found
that specific patterns of [Ca2+](i) elevation selectively activate LTP or L
TD. In particular, only LTP was triggered by a brief increase of [Ca2+](i)
with relatively high magnitude, which mimics the [Ca2+](i) rise during elec
trical stimulation typically used to induce LTP. In contrast, a prolonged m
odest rise of [Ca2+](i) reliably induced LTD. An important implication of t
he results is that both the amplitude and the duration of an intracellular
chemical signal can carry significant biological information.