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R. Rajan, P.B. Cook; Amacrine Cells Can Intrinsically Fire Repetitive Action Potentials . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2334.
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© ARVO (1962-2015); The Authors (2016-present)
Background: Amacrine cells (ACs) in the inner retina mediate transient and sustained inhibition. The lateral transmission of both types of inhibitory signals require action potentials. Action potentials in transient ACs are well documented, and have been explained by properties of intrinsic membrane channels, and alternatively by network interactions. Presumably, sustained responding amacrine cells fire trains of action potentials, but physiological evidence from salamander retina, the species used in this study, has been weak. Purpose:The purpose of this study was to examine the spiking behavior of ACs to steps of depolarizing current, to determine if the they can spike repetitively, and to determine if their spiking behavior is dependent on synaptic interactions or is a result of intrinsic membrane channels. Methods: 300 um thick retinal slices were prepared from larval tiger salamanders. Cell–attached currents and whole–cell voltages were recorded from amacrine cells to observe spike activity in response to voltage steps and current injections, respectively. Intrinsic spike–activity was observed by synaptically isolating the amacrine cells using d–AP5 [50 uM], DNQX [100 uM], strychnine [10 uM] and bicuculline [100 uM]. Subsequently, amacrine cells were exposed cadmium [200 uM] to observe calcium–dependent attributes of repetitive firing. Results: Cell–attached recordings showed that a majority of cells fired action potentials repetitively during step depolarizations in control Ringer's, and also after postsynaptic receptors were blocked. In whole–cell recording mode, cells that fired repetitively exhibited both fast (tau rise 3.46+/– 2.44 msec) and slower regenerative potentials (tau rise 62.8 +/– 19.2 msec). Only the slow potentials were blocked by the addition of cadmium. In a few cells cadmium also blocked repetitive firing of fast action potentials. Some ACs that responded transiently to depolarizing steps, remained transient after synaptic inputs were blocked, while other transient ACs began to spike repetitively. Conclusions: The overwhelming majority of cells fired repetitive action potentials in response to step depolarizations in both control, and in the absence of synaptic transmission. Transiently responding amacrine cells either remained transient or fired trains of action potentials when synaptic input was blocked, supporting both the intrinsic and the network models explaining mechanisms underlying transient inhibition.
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