We have used confocal microscopy to monitor synaptically evoked Ca2+ transients in the dendritic spines of hippocampal pyramidal cells. Individual spines respond to single afferent stimuli (<0.1 Hz) with Ca2+ transients or failures, reflecting the probability of transmitter release at the activated synapse. Both AMPA and NMDA glutamate receptor antagonists block the synaptically evoked Ca2+ transients; the block by AMPA antagonists is relieved by low Mg2+. The Ca2+ transients are mainly due to the release of calcium from internal stores, since they are abolished by antagonists of calcium-induced calcium release (CICR); CICR antagonists, however, do not depress spine Ca2+ transients generated by backpropagating action potentials. These results have implications for synaptic plasticity, since they show that synaptic stimulation can activate NMDA receptors, evoking substantial Ca2+ release from the internal stores in spines without inducing long-term potentiation (LTP) or depression (LTD).
Journal article
1999-01-01T00:00:00+00:00
22
115 - 124
9
6-Cyano-7-nitroquinoxaline-2,3-dione, Animals, Calcium, Dendrites, Electric Conductivity, Enzyme Inhibitors, Excitatory Amino Acid Antagonists, Hippocampus, Indoles, Male, Rats, Rats, Wistar, Receptors, N-Methyl-D-Aspartate, Ryanodine, Synapses