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. 1986 Mar;83(5):1509-12.
doi: 10.1073/pnas.83.5.1509.

Gated currents generate single spike activity in amacrine cells of the tiger salamander retina

Gated currents generate single spike activity in amacrine cells of the tiger salamander retina

S Barnes et al. Proc Natl Acad Sci U S A. 1986 Mar.

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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References

    1. Science. 1972 Mar 3;175(4025):1008-10 - PubMed
    1. J Gen Physiol. 1974 Jan;63(1):88-110 - PubMed
    1. J Neurocytol. 1974 Mar;3(1):1-33 - PubMed
    1. Brain Res. 1976 Mar 5;104(1):157-62 - PubMed
    1. J Physiol. 1977 Jan;264(3):767-85 - PubMed

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