Calcium signals in long-term potentiation and long-term depression

We describe postsynaptic Ca2+ signals that subserve induction of two forms of neuronal plasticity, long-term potentiation (LTP) and long-term depressi on (LTD), in rat hippocampal neurons. The common induction protocol for LTP , a 1-s, 50-Hz tetanus, generates Ca2+ increases of about 50 mu M in dendri tic spines of CA1 neurons. These very large increases, measured using a low affinity indicator (Mg fura 5), were found only in the spines and tertiary dendrites, and were dependent upon influx through N-methyl-D-aspartate (NM DA) gated channels. High affinity Ca2+ indicators (e.g., fura 2) are unable to demonstrate these events. In acute slices, neighboring dendritic branch es often showed very different responses to a tetanus, and in some instance s, neighboring spines on the same dendrite responded differently. LTD in ma ture CA1 neurons was induced by a low frequency stimulus protocol (2 Hz, 90 0 pulses), in the presence of GABA- and NMDA-receptor blockers. This LTD pr otocol produced dendritic Ca2+ increases of < 1 mu M. Duration of the Ca2increase was similar to 30 s and was due to voltage-gated Ca2+ influx. Fina lly, the ability of synaptically addressed Ca2+ stores to release Ca2+ was studied in CA3 neurons and was found to require immediate preloading and hi gh intensity presynaptic stimulation, conditions unlike normal LTP-LTD prot ocols.