There are 3 known forms of synaptic plasticity at CNS synapses: long-t
erm potentiation (LTP) mediated by NMDA receptor activation, LTP media
ted by voltage-dependent calcium channel (VDCC) activation, and long-t
erm depression (LTD) mediated by the NMDA receptor. All 3 forms of syn
aptic plasticity can be observed in hippocampal CA1 cells, all are ind
uced by afferent activation, all involve Ca2+ influx, and all activate
Ca2+-dependent mechanisms. We consider the functional consequences of
the presence of 3, sometime opposing, forms of synaptic plasticity at
the same synapse. We suggest that the 2 forms of LTP have different c
onsequences for the synapse. We postulate that the co-existence of pot
entiating and depressing capabilities influences the network processin
g capabilities of neural networks.