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K + ‐Evoked Depolarization Stimulates Cyclic AMP Accumulation in Photoreceptor‐Enriched Retinal Cell Cultures: Role of Calcium Influx Through Dihydropyridine‐Sensitive Calcium Channels
Author(s) -
Iuvone P. Michael,
Gan Jiwei,
Avendano Gary
Publication year - 1991
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1991.tb03792.x
Subject(s) - depolarization , dihydropyridine , biophysics , nifedipine , calcium , stimulation , extracellular , membrane potential , chemistry , voltage dependent calcium channel , intracellular , channel blocker , biology , endocrinology , medicine , biochemistry , organic chemistry
The effect of membrane depolarization on cyclic AMP synthesis was studied in glia‐free, low‐density, mono‐layer cultures of chick retinal photoreceptors and neurons. In photoreceptor‐enriched cultures prepared from embryonic day 6 retinas and cultured for 6 days, elevated K + concentrations increased the intracellular concentration of cyclic AMP and stimulated the conversion of [ 3 H]adenine to [ 3 H]cyclic AMP. The K + ‐evoked increase of cyclic AMP accumulation was blocked by omitting CaCl 2 from the incubation medium, indicating a requirement for extracellular Ca 2+ . Stimulation of cyclic AMP accumulation was also inhibited by nifedipine, methoxyverapamil, Cd 2+ , Co 2+ , and Mg 2+ , and was enhanced by the dihydropyridine Ca 2+ channel agonist Bay K 8644. The enhancement of K + ‐evoked cyclic AMP accumulation by Bay K 8644 was antagonized by nifedipine. Thus, Ca 2+ influx through dihydropyridine‐sensitive channels is required for depolarization‐evoked stimulation of cyclic AMP accumulation in photoreceptor‐enriched cultures.