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Department of Physiology and Biophysics, School of Medicine, State University of New York at Buffalo, Buffalo, NY 14214

Address correspondence to Malcolm Slaughter, Department of Physiology and Biophysics, University at Buffalo, 124 Sherman Hall Buffalo, NY 14214. Tel.: (716) 829-3240; Fax: (716) 829-2344; E-mail: mslaught{at}buffalo.edu

Spontaneous miniature outward currents (SMOCs) occur in a subset of retinal amacrine cells at membrane potentials between -60 and -40 mV. At more depolarized potentials, a transient outward current (I_to) appears and SMOCs disappear. Both SMOCs and the I_to are K⁺ currents carried by BK channels. They both arise from Ca²⁺ influx through high voltage–activated (HVA) Ca²⁺ channels, which stimulates release of internal Ca²⁺ from caffeine- and ryanodine-sensitive stores. An increase in Ca²⁺ influx resulted in an increase in SMOC frequency, but also led to a decline in SMOC mean amplitude. This reduction showed a temporal dependence: the effect being greater in the latter part of a voltage step. Thus, Ca²⁺ influx, although required to generate SMOCs, also produced a negative modulation of their amplitudes. Increasing Ca²⁺ influx also led to a decline in the first latency to SMOC occurrence. A combination of these effects resulted in the disappearance of SMOCs, along with the concomitant appearance of the I_to at high levels of Ca²⁺ influx. Therefore, low levels of Ca²⁺ influx, arising from low levels of activation of the HVA Ca²⁺ channels, produce randomly occurring SMOCs within the range of -60 to -40 mV. Further depolarization leads to greater activation of the HVA Ca²⁺ channels, larger Ca²⁺ influx, and the disappearance of discontinuous SMOCs, along with the appearance of the I_to. Based on their characteristics, SMOCs in retinal neurons may function as synaptic noise suppressors at quiescent glutamatergic synapses.

Key Words: BK channels • ryanodine receptors • transient potassium current • ganglion cells • dihyropyridines

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