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 depression (LTD), in rat hippocampal neurons. The common induction protocol for LTP, a 1-s, 50-Hz tetanus, generates Ca2+ increases of about 50-Hz in dendritic 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 (NMDA) gated channels. High affinity Ca2+ indicators (e.g., fura 2) are unable to demonstrate these events. In acute slices, neighboring dendritic branches often showed very different responses to a tetanus, and in some instances, neighboring spines on the same dendrite responded differently. LTD in mature CA1 neurons was induced by a low frequency stimulus protocol (2 Hz, 900 pulses), in the presence of GABA- and NMDA-receptor blockers. This LTD protocol produced dendritic Ca2+ increases of <1 microM. Duration of the Ca2+ increase was approximately 30 s and was due to voltage-gated Ca2+ influx. Finally, the ability of synaptically addressed Ca2+ stores to release Ca2+ was studied in CA3 neurons and was found to require immediate preloading and high intensity presynaptic stimulation, conditions unlike normal LTP-LTD protocols.
Connor
J A
JA
Department of Neuroscience, University of New Mexico School of Medicine, Albuquerque 87131, USA.
Petrozzino
J
J
Pozzo-Miller
L D
LD
Otani
S
S
D000818:Animals; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling; D006624:Hippocampus / Q000502:physiology*; D017774:Long-Term Potentiation; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology; D013569:Synapses / Q000502:physiology
D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium