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 ω-conotoxin MVIIA (1 μM) nor ω-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.
Dendritic branch-constrained NMDA spikes drive synaptic plasticity in hippocampal CA3 pyramidal cells
