Abstract
Amacrine cells form the neural networks mediating the second level of lateral interactions in the vertebrate retina. Members of a prominent class of amacrine cells, found in most vertebrates, respond at both the onset and termination of steps of illumination with a single, large transient depolarization. We show here how specific relationships between membrane currents control this single spike activity. Using whole-cell patch clamp on living retinal slices, we studied the membrane currents in amacrine cells. The currents elicited by depolarizing voltage steps could be separated into three main ionic components: a transient inward voltage-gated sodium current, a relatively small sustained inward voltage-gated calcium current, and a calcium-dependent outward current. A specific relationship between the sodium and potassium current alone appears to preclude repetitive spike activity. Potassium current is activated at potentials positive to -20 mV, but the sodium inactivation, between -60 and -20 mV, does not intersect potassium activation. Therefore, a steady depolarizing current step elicits an initial spike but then the membrane cannot be sufficiently hyperpolarized by potassium current to remove sodium inactivation and the cell remains refractory.
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Selected References
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