Persistent Na+ current and Ca2+ current boost graded depolarization of ratretinal amacrine cells in culture

Retinal amacrine cells are depolarized by the excitatory synaptic input fro m 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 (T TX). In the present study, we investigated the contribution of voltage-gate d currents to membrane depolarization by using rat GABAergic amacrine cells in culture recorded by the patch-clamp method. Injection of a negative cur rent induced membrane hyperpolarization, the waveform of which can be well fitted by a single exponential function. Injection of positive current depo larized the cell, and the depolarization exceeded the amplitude expected fr om the passive properties of the membrane. The boosted depolarization susta ined after the current was turned off. Either 1 muM TTX or 2 mM Co2+ suppre ssed the boosted depolarization, and co-application of TTX and Co2+ blocked it completely. Under the voltage clamp, we identified a transient Na+ curr ent (fast I-Na), a TTX-sensitive persistent current that reversed the polar ity near the equilibrium potential of Na+ (I-NaP), and three types of Ca2currents (I-Ca), L, N, and the pharmacological agent-resistant type (R type ). These findings suggest that the I-NaP and I-Ca of amacrine cells boost d epolarization evoked by the excitatory synaptic input, and they may aid the spread of electrical signals among dendritic arbors of amacrine cells.