Localized contribution of N-methyl-D-aspartate receptors to synaptic input-induced rise of calcium in apical dendrites of layer II/III neurons in rat visual cortex.
To examine the role of N-methyl-D-aspartate receptors in the synaptic input-induced increase in Ca2+ in layer II/III neurons of visual cortex, Ca2+ imaging with a relatively low-affinity indicator was carried out simultaneously with whole-cell recordings of synaptic activity in cortical slices of young rats. Electrical stimulation of layer IV elicited excitatory postsynaptic potentials that generated action potentials concomitantly with a marked rise of Ca2+ signal in apical dendrites of 24 pyramidal cell-like neurons. Dendritic regions about 50 microm from the soma (peak regions) consistently showed the strongest increase in signal. The application of an N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphonovalerate, reduced the Ca2+ signal in peak regions but did not in other regions in nine of the 15 neurons tested. In all the dendritic regions in which Ca2+ signal was measured, the magnitude of the increase in signal was related linearly to the number of action potentials, suggesting that voltage-dependent Ca2+ channels activated by action potentials may also be involved in the increase. In 25 of 33 neurons which were voltage-clamped at 80 mV and perfused with the Mg2+-free solution, layer IV stimulation could induce a local rise in Ca2+ signal in apical dendrites. This rise was blocked by the N-methyl-D-aspartate receptor antagonist almost completely. Such an antagonist-sensitive Ca2+ rise was still seen even when the membrane potential was held at +10 mV when voltage-dependent Ca2+ channels were expected not to be activated by excitatory synaptic inputs. These results suggest that N-methyl-D-aspartate receptors are involved in the synaptic input-induced rise in Ca2+ at postsynaptic sites in apical dendrites of layer II/III neurons, and the increase may be boosted through voltage-dependent Ca2+ channels activated by action potentials.
Department of Neurophysiology, Biomedical Research Center, Osaka University Medical School, Suita City, Japan.
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Yasuda
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Kinoshita
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Tsumoto
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003712:Dendrites / Q000378:metabolism* / Q000648:ultrastructure; D004594:Electrophysiology; D005456:Fluorescent Dyes; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000502:physiology; D009476:Neurons, Efferent / Q000378:metabolism* / Q000648:ultrastructure; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects; D014793:Visual Cortex / Q000378:metabolism* / Q000648:ultrastructure
D005456:Fluorescent Dyes; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium