Dihydropyridine-sensitive, voltage-gated Ca^2+ channels contribute to the
resting intracellular Ca^2+ concentration of hippocampal CA1 pyramidal
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