|
|
|
|
|
|
|
||
The Journal of General Physiology, Vol 101, 695-714, Copyright © 1993 by The Rockefeller University Press
ARTICLES |
K Takahashi, DB Dixon and DR Copenhagen
Department of Ophthalmology, University of California, San Francisco 94143-0730.
A sustained high voltage-activated (HVA), nifedipine- and cadmium- sensitive calcium current and a sustained calcium action potential (AP) were recorded from horizontal cells isolated from catfish retina. pH indicator dyes showed that superfusion with NH4Cl alkalinized these cells and that washout of NH4Cl or superfusion with Na-acetate acidified them. HVA current was slightly enhanced during superfusion of NH4Cl but was suppressed upon NH4Cl washout or application of Na- acetate. When 25 mM HEPES was added to the patch pipette to increase intracellular pH buffering, the effects of NH4Cl and Na-acetate on HVA current were reduced. These results indicated that intracellular acidification reduces HVA calcium current and alkalinization increases it. Sustained APs, recorded with high resistance, small diameter microelectrodes, were blocked by cobalt and cadmium and their magnitude varied with extracellular calcium concentration. These results provide confirmatory evidence that the HVA current is a major component of the AP and indicate that the AP can be used as a measure of how the HVA current can be modified in intact, undialyzed cells. The duration of APs was increased by superfusion with NH4Cl and reduced by washout of NH4Cl or superfusion with Na-acetate. The Na-acetate and NH4Cl washout- dependent shortening of the APs was observed in the presence of intracellular BAPTA, a calcium chelator, IBMX, a phosphodiesterase inhibitor, and in Na-free or TEA-enriched saline. These findings provide supportive evidence that intracellular acidification may directly suppress the HVA calcium current in intact cells. Intracellular pH changes would thereby be expected to modulate not only the resting membrane potential of these cells in darkness, but calcium- dependent release of neurotransmitter from these cells as well. Furthermore, this acidification-dependent suppression of calcium current could serve a protective role by reducing calcium entry during retinal ischemia, which is usually thought to be accompanied by intracellular acidosis.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  M. G. Jonz and S. Barnes Proton modulation of ion channels in isolated horizontal cells of the goldfish retina J. Physiol., June 1, 2007; 581(2): 529 - 541. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Checchin, X. Hou, P. Hardy, D. Abran, T. Najarian, M. H. Beauchamp, S. G. Bernier, F. Gobeil Jr, C. Quiniou, D. R. Varma, et al. PGE2-Mediated eNOS Induction in Prolonged Hypercapnia Invest. Ophthalmol. Vis. Sci., May 1, 2002; 43(5): 1558 - 1566. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L.-E. Trudeau, V. Parpura, and P. G. Haydon Activation of Neurotransmitter Release in Hippocampal Nerve Terminals During Recovery From Intracellular Acidification J Neurophysiol, June 1, 1999; 81(6): 2627 - 2635. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Kiss and S. J. Korn Modulation of N-Type Ca2+ Channels by Intracellular pH in Chick Sensory Neurons J Neurophysiol, April 1, 1999; 81(4): 1839 - 1847. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. B. Thoreson, R. Nitzan, and R. F. Miller Reducing Extracellular Cl- Suppresses Dihydropyridine-Sensitive Ca2+ Currents and Synaptic Transmission in Amphibian Photoreceptors J Neurophysiol, April 1, 1997; 77(4): 2175 - 2190. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. C. Tombaugh and G. G. Somjen Differential Sensitivity to Intracellular pH Among High- and Low-Threshold Ca2+ Currents in Isolated Rat CA1 Neurons J Neurophysiol, February 1, 1997; 77(2): 639 - 653. [Abstract] [Full Text] [PDF]
|
|
|
|
