Transduction persists in rod photoreceptors after depletion of intracellular calcium

Grant Nicol, U. B. Kaupp, M. D. Bownds

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

We have examined the role of Ca++ in phototransduction by manipulating the intracellular Ca++ concentration in physiologically active suspensions of isolated and purified rod photoreceptors (OS-IS). The results are summarized by the following. (a) Measurement of Ca++ content using arsenazo III spectroscopy demonstrates that incubation of OS-IS in 10 nM Ca++-Ringer's solution containing the Ca++ ionophore A23187 reduced their Ca++ content by 93%, from 1.3 to 0.1 mol Ca++/mol rhodopsin. Virtually the same reduction can be accomplished in 10 nM Ca++-Ringer's without ionophore, presumably via the plasma membrane Na/Ca exchange mechanism. (b) Hundreds of photoresponses can be obtained from the Ca++-depleted OS-IS for at least 1 h in 10 nM Ca++-Ringer's with ionophore. The kinetics and light sensitivity of the photoresponse are essentially the same in the presence or absence of the ionophore in 10 nM Ca++. (c) The addition of A23187 in 1 mM Ca++-Ringer's results in a Ca++ influx that rapidly suppresses the dark current and the photoresponse. This indicates that there is an intracellular site at which Ca++ can modulate the light-regulated conductance. Both the current and photoresponse can be restored if intracellular Ca++ is reduced by lowering the external Ca++ to 10 nM. During the transition from high to low Ca++, the response duration becomes shorter, which suggests that it can be regulated by a Ca++-dependent mechanism. (d) If the dark current and the photoresponse are suppressed by adding A23187 in 1 mM Ca++-Ringer's, the subsequent addition of the cyclic GMP phosphodiesterase inhibitor isobutylmethylxanthine can restore the current and photoresponse. This implies that under conditions where the rod can no longer control its intracellular Ca++, the elevation of cyclic GMP levels can restore light regulation of the channels. The persistance of normal flash responses under conditions where intracellular Ca++ levels are reduced and perturbed suggests that changes in the intracellular Ca++ concentration do not cause the closure of the light-regulated channel.

Original languageEnglish (US)
Pages (from-to)297-319
Number of pages23
JournalJournal of General Physiology
Volume89
Issue number2
StatePublished - 1987
Externally publishedYes

Fingerprint

Retinal Rod Photoreceptor Cells
Ionophores
Calcimycin
Calcium
Cyclic GMP
Light
Arsenazo III
Light Signal Transduction
Photophobia
Rhodopsin
Phosphodiesterase Inhibitors
Spectrum Analysis
Suspensions
Cell Membrane

ASJC Scopus subject areas

  • Physiology

Cite this

Transduction persists in rod photoreceptors after depletion of intracellular calcium. / Nicol, Grant; Kaupp, U. B.; Bownds, M. D.

In: Journal of General Physiology, Vol. 89, No. 2, 1987, p. 297-319.

Research output: Contribution to journalArticle

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