Identified wind-sensitive giant interneurons in the cricket's cercal sensory system integrate cercal afferent signals and release an avoidance behavior. A calcium-imaging technique was applied to the giant interneurons to examine the presence of the voltage-dependent Ca2+ channels (VDCCs) in their dendrites. We found that presynaptic stimuli to the cercal sensory nerve cords elevated the cytosolic Ca2+ concentration ([Ca2+](i) in the dendrites of the giant interneurons. The dendritic Ca2+ rise coincided with the spike burst of the giant interneurons, and the rate of Ca2+ rise depended on the frequency of the action potentials. These results suggest that the action potentials directly caused [Ca2+](i) increase. Observation of the [Ca2+](i) elevation induced by depolarizing current injection demonstrates the presence of the VDCCs in the dendrites. Although hyperpolarizing current injection into the giant interneuron suppressed action potential generation, EPSPs could induce no [Ca2+](i) increase. This result means that ligand-gated channels do not contribute to the synaptically stimulated Ca2+ elevation. On the other hand, antidromically stimulated spikes also increased [Ca2+](i) in all cellular regions including the dendrites. And bath application of a mixture of Ni2+, Co2+, and Cd2+ or tetrodotoxin inhibited the [Ca2+](i) elevation induced by the antidromic stimulation. From these findings, we suppose that the axonal spikes antidromically propagate and induce the Ca2+ influx via VDCCs in the dendrites. The spike-dependent Ca2+ elevation may regulate the sensory signals processing via second-messenger cascades in the giant interneurons. (C) 2000 John Wiley and Sons. Inc.
|ジャーナル||Journal of Neurobiology|
|出版ステータス||Published - 2000|
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