Dihydropyridine-sensitive, voltage-gated Ca^2+ channels contribute to the resting intracellular Ca^2+ concentration of hippocampal CA1 pyramidal neurons. Magee, Jeffrey C., Robert B. Avery, Brian R. Christie and Daniel Johnston. Division of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030.
APStracts 3:0131N, 1996.
SUMMARY AND CONCLUSIONS
1. Whole-cell recordings and high-speed fluorescence imaging were used to investigate the contribution of voltage-gated Ca^2+ channels to the resting Ca^2+ concentration ([Ca^2+]_i) in hippocampal CA1 pyramidal neurons. 2. Prolonged membrane hyperpolarization produced, in a voltage-dependent manner, sustained decreases in [Ca^2+]_i in the somatic and apical dendritic regions of the neuron. This hyperpolarization-induced decrease in [Ca^2+]_i occurred with a time constant of approximately 1 sec and was maintained for as long as the membrane potential was held at the new level. Ratiometric measures showed that [Ca^2+]_i is significantly elevated at holding potentials of -50 mV compared to -80 mV. 3. The hyperpolarization-induced decrease in [Ca^2+]_i was significantly reduced by 200 muM Cd^2+ and 10 muM Nimodipine, but was only slightly inhibited by 50 muM Ni^2+. The largest amplitude decrease in [Ca^2+]_i was observed in the proximal apical dendrites with the amplitude of the Ca^2+ change decreasing with further distance from the soma. 4. Whole-cell recordings from acutely isolated hippocampal pyramidal neurons reveal a slowly inactivating Ca^2+ current with similar voltage-dependence and pharmacology to the hyperpolarization-induced decrease in [Ca^2+]_i. 5. The data suggest that a population of dihydropyridine-sensitive Ca^2+ channels are active at resting membrane potentials and that this channel activation significantly contributes to the resting [Ca^2+]_i. These channels appear to be present throughout the neuron and may be most densely located in the proximal apical dendrites.

Received 18 March 1996; accepted in final form 30 May 1996.
APS Manuscript Number J224-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 28 June 96