Reducing extracellular Cl- suppresses dihydropyridine-sensitive Ca++
currents and synaptic transmission in amphibian photoreceptors.
Wallace B. Thoreson, Ron Nitzan, and Robert F. Miller.
Departments of Ophthalmology and Pharmacology, Gifford Laboratory of
Ophthalmology, University of Nebraska Medical Center, Omaha, NE 68198-5540.
Department of Physiology, University of Minnesota, Minneapolis, MN 55455.
APStracts 4:0006N, 1997.
ABSTRACT
Areduction 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 Ca++ (Fura-2)
and pH (BCECF) in dissociated photoreceptors. The results show that reducing
extracellular Cl- suppresses a dihydropyridine (DHP)-sensitive Ca++ 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 Ca++ channels which 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 Ca++ channels in
photoreceptors and, hence, photoreceptor function.
Received 15 July 1996; accepted in final form 20 December 1996.
APS Manuscript Number J556-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 21 January 1997