The Journal of Neurophysiology Vol. 80 No. 5 November 1998, pp. 2268-2273
Copyright ©1998 The American Physiological Society

L-Type Ca²⁺ Channels Mediate the Slow Ca²⁺-Dependent Afterhyperpolarization Current in Rat CA3 Pyramidal Cells In Vitro

Mitsuo Tanabe, Beat H. Gähwiler, and Urs Gerber

Brain Research Institute, University of Zurich, CH-8057 Zurich, Switzerland

Tanabe, Mitsuo, Beat H. Gähwiler, and Urs Gerber. L-type Ca²⁺ channels mediate the slow Ca²⁺-dependent afterhyperpolarization current in rat CA3 pyramidal cells in vitro. J. Neurophysiol. 80: 2268-2273, 1998. Single-electrode voltage-clamp recordings were obtained from CA3 pyramidal cells in rat hippocampal organotypic slice cultures, and the slow Ca²⁺-dependent K⁺ current or afterhyperpolarization current (I_AHP) was elicited with brief depolarizing voltage jumps. The slow I_AHP was suppressed by the selective L-type Ca²⁺ channel antagonists isradipine (2 µM) or nifedipine (10 µM). In contrast, neither -conotoxin MVIIA (1 µM) nor -agatoxin IVA (200 nM), N-type and P/Q-type Ca²⁺ channel antagonists, respectively, attenuated this slow outward current. The slow I_AHP was significantly reduced by thapsigargin (10 µM), a Ca²⁺ ATPase inhibitor that depletes intracellular Ca²⁺ stores, and by ryanodine (10-100 µM), which blocks Ca²⁺-induced Ca²⁺ release from intracellular compartments. At this concentration thapsigargin did not modify high-threshold Ca²⁺ current, which was, however, blocked by isradipine. Thus, in hippocampal CA3 pyramidal cells, Ca²⁺ influx through L-type Ca²⁺ channels is necessary to trigger the slow I_AHP. Furthermore, intracellular Ca²⁺-activated Ca²⁺ stores represent a critical component in the transduction pathway leading to the generation of the slow I_AHP.

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