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Spike-induced calcium signals and afterhyperpolarizations in neocortical pyramidal neurons



Spike-induced calcium signals and afterhyperpolarizations in neocortical pyramidal neurons



Society for Neuroscience Abstracts 27(1): 1004



In neocortical pyramidal cells, Ca2+ entry through voltage-gated channels during repetitive firing activates Ca2+-dependent K+ channels, resulting in an afterhyperpolarization (AHP) which is an important negative regulator of the cell's firing behavior (e.g., spike frequency adaption). This AHP consists of an apamin-sensitive medium component (mAHP) and an apamin-insensitive slow component (sAHP). These two AHP components differ in decay kinetics. The spike-induced build-up of (Ca2+)i may also serve to monitor the cell's activity and control cellular processes such as gene transcription. Using whole-cell patch recording from slices of rat somatosensory neocortex with simultaneous fura-2 Ca2+ imaging, we determined the relationships between (1) the frequency and number of spikes and the amplitudes of the mAHP and sAHP and (2) between the frequency and number of spikes and (Ca2+)i in soma and dendrites. The mAHP was present after one spike but the sAHP required several spikes to be measurable. Both AHPs increased in size with additional spikes until a plateau level was reached. We found that (Ca2+)i in the proximal dendrites reaches a steady-state plateau whose amplitude is dependent on spike frequency (cf., Helmchen et al. (1996) Biophys. J. 70:1069-1081). However, our data suggest that this relationship is exponential rather than linear. Finally, we compared the time course of (Ca2+)i decay with the time courses of the sAHP and mAHP to examine compartmentalization as a possible explanation for differences in kinetics between the two AHPs.

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