TRANSIENT AND SUSTAINED DEPOLARIZATION OF RETINAL GANGLION CELLS BY Ih.
Tabata, Toshihide & Andrew T. Ishida.
Section of Neurobiology, Physiology, and Behavior, University of
California, Davis, CA 95616-8519.
APStracts 2:0362N, 1995.
SUMMARY AND CONCLUSIONS
1) Using whole-cell patch-clamp methods, we have identified an inward cationic
current activated by hyperpolarization (I h ) in somata of goldfish retinal
ganglion cells. 2) I h activated at test potentials between -70 mV and -105
mV, and did not appear to inactivate during prolonged hyperpolarizations under
voltage clamp. During step hyperpolarizations from holding potentials between
-70 mV and -40 mV, apparent activation was faster at more negative test
potentials. Upon repolarization from -105 mV to holding potentials between -75
mV and -55 mV, I h deactivated exponentially at rates showing no marked
voltage-dependence ([tau] = ca. 100 msec). 3) I h tail currents reversed at
membrane potentials consistent with a relative permeability to Na + and K + (P
Na /P K ) of roughly 0.5, when pipet and bath solutions both contained Na +
and K + . 4) I h was readily blocked by extracellular Cs + (3 mM), but was
resistant to block by tetraethylammonium (30 mM), Ba 2+ (1 mM), or Co 2+ (2.4
mM). 5) Time-dependent voltage-rectification developed during injection of
hyperpolarizing current under current clamp. After current injection ceased,
membrane potential depolarized beyond resting potential, often leading to
anode-break-like spikes. Both voltage-rectification and voltage-overshoot were
suppresed by extracellular Cs + . 6) Voltage-clamp measurements in the
presence and absence of Cs + were used to model membrane potential changes
produced by exogenous current injections, by hyperpolarizing synaptic inputs,
and by termination of both. Modeled responses resembled membrane potential
changes measured under current clamp when terms for activation and
deactivation of I h were included. 7) The voltage rectification and anode-
break-like spikes observed in isolated cells resembles those recorded during
and after light-evoked hyperpolarizations of retinal ganglion cells in situ. I
h may transiently augment retinal ganglion cell excitability after termination
of hyperpolarizing light stimuli, and thus promote encoding of stimulus
timing.
Received 9 November 1995; accepted in final form 9 November 1995.
APS Manuscript Number J707-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95