Voltage dependent L-type Ca
2+ channels present at neuron axon terminals are quite sensitive to a slight pH change of external medium at the physiological pH range. Proton (H
+) released from depolarised horizontal cells (HCs) in the retina is assumed to act as an inhibitory transmitter via the Ca
2+ channels on glutamate release from photoreceptor terminals, contributing to improvement of spatial contrast based on centre-surround antagonistic receptive field in visual functions. I will discuss this negative feedback processing due to the mechanisms of plasmalemma V-ATPase, a molecular machinery working as an H
+ pump, acting to extrude/intrude H
+ at plasma membrane. H
+ concentration nearby the external membrane surface could be controlled by the H
+ pump driven by the ATP hydrolysis and proton motive force (pmf) based on the difference between the membrane potential and H
+ reversal potential. The pmf can be a candidate for a rapid pH controlling mechanism of nervous systems at the synaptic cleft without dependent on ATP hydrolysis. Possible roles of small molecules, nitric oxide and hydrogen sulphide, were also discussed on the control of retinal neurones by the V-ATPase modulation.
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