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Suppresses Dihydropyridine-Sensitive Ca2+ Currents and Synaptic Transmission in Amphibian Photoreceptors
1 Departments of Ophthalmology and Pharmacology, Gifford Laboratory of Ophthalmology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5540; and 2 Department of Physiology, University of Minnesota, Minneapolis, Minnesota 55455
Thoreson, Wallace B., Ron Nitzan, and Robert F. Miller. Reducing extracellular Cl
suppresses dihydropyridine-sensitive Ca2+ currents and synaptic transmission in amphibian photoreceptors. J. Neurophysiol. 77: 2175-2190, 1997. A reduction in extracellular chloride suppresses light-evoked currents of second-order retinal neurons (bipolar and horizontal cells) by reducing release of glutamate from photoreceptors. The underlying mechanisms responsible for this action of reduced extracellular Cl were studied with a combination of electrophysiological recordings from single neurons in a retinal slice preparation and image analyses of intracellular Ca2+ (Fura-2) and pH [2
,7-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein, acetoxymethyl ester] in dissociated photoreceptors. The results show that reducing extracellular Cl suppresses a dihydropyridine (DHP)-sensitive Ca2+ current (ICa) in photoreceptors. It is proposed that suppression of ICa results in suppression of photoreceptor neurotransmission. The suppressive effect of low Cl on ICa is not due to antagonism by the substituting anion nor is it mediated by changes in extracellular or intracellular pH. We conclude that normal extracellular levels of Cl are important for maintenance of the voltage-gated Ca2+ channels that support neurotransmission from photoreceptors. Several ideas are presented about the mechanisms by which Cl supports photoreceptor neurotransmission and the possibility that modulations of Cl might play a physiological role in the regulation of Ca2+ channels in photoreceptors and, hence, photoreceptor function.
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