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The Journal of Neurophysiology Vol. 86 No. 2 August 2001, pp. 1006-1016
Copyright ©2001 by the American Physiological Society
Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan
Koizumi, Amane,
Shu-Ichi Watanabe, and
Akimichi Kaneko.
Persistent Na+ Current and Ca2+ Current
Boost Graded Depolarization of Rat Retinal Amacrine Cells in Culture. J. Neurophysiol. 86: 1006-1016, 2001. Retinal amacrine cells are
depolarized by the excitatory synaptic input from bipolar cells. When a
graded depolarization exceeds the threshold level, trains of action
potentials are generated. There have been several reports that both
spikes and graded depolarization are sensitive to tetrodotoxin (TTX).
In the present study, we investigated the contribution of voltage-gated
currents to membrane depolarization by using rat GABAergic amacrine
cells in culture recorded by the patch-clamp method. Injection of a
negative current induced membrane hyperpolarization, the waveform of
which can be well fitted by a single exponential function. Injection of positive current depolarized the cell, and the depolarization exceeded
the amplitude expected from the passive properties of the membrane. The
boosted depolarization sustained after the current was turned off.
Either 1 µM TTX or 2 mM Co2+ suppressed the
boosted depolarization, and co-application of TTX and
Co2+ blocked it completely. Under the voltage
clamp, we identified a transient Na+ current
(fast INa), a TTX-sensitive persistent
current that reversed the polarity near the equilibrium potential of
Na+ (INaP), and
three types of Ca2+ currents
(ICa), L, N, and the pharmacological
agent-resistant type (R type). These findings suggest that the
INaP and
ICa of amacrine cells boost
depolarization evoked by the excitatory synaptic input, and they may
aid the spread of electrical signals among dendritic arbors of amacrine cells.
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