TRANSIENT AND SUSTAINED DEPOLARIZATION OF RETINAL GANGLION-CELLS BY I-H

1. Using whole cell patch-clamp methods, we have identified an inward cationic current activated by hyperpolarization (I-h) in somata of gol dfish retinal ganglion cells. 2. I-h activated at test potentials betw een -70 and -105 mV, and did not appear to inactivate during prolonged hyperpolarizations under voltage clamp. During step hyperpolarization s from holding potentials between -70 and -40 mV, apparent activation was faster at more negative test potentials. On repolarization from -1 05 mV to holding potentials between -75 and -55 mV, I-h deactivated ex ponentially at rates showing no marked voltage dependence (tau = simil ar to 100 ms). 3. I-h tail currents reversed at membrane potentials co nsistent with a relative permeability to Na+ and K+ of roughly 0.5, wh en pipette and bath solutions both contained Na+ and K+. 4. I-h was re adily blocked by extracellular Cs+ (3 mM), but was resistant to block by tetraethylammonium (30 mM), Ba2+ (1 mM), or Co2+ (2.4 mM). 5. Time- dependent voltage rectification developed during injection of hyperpol arizing current under current clamp. After current injection ceased, m embrane potential depolarized beyond resting potential, often leading to anode-break-like spikes. Both voltage rectification and voltage ove rshoot were suppressed by extracellular Cs+. 6. Voltage-clamp measurem ents in the presence and absence of Cs+ were used to model membrane po tential changes produced by exogenous current injections, by hyperpola rizing 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 vo ltage rectification and anode-break-like spikes observed in isolated c ells resemble those recorded during and after light-evoked hyperpolari zations of retinal ganglion cells in situ. I-h may transiently augment retinal ganglion cell excitability after termination of hyperpolarizi ng light stimuli, and thus promote encoding of stimulus timing.