当前位置： SCI文献检索 > NEUROCHEMISTRY INTERNATIONAL期刊下所有文献 > K(+)-evoked depolarization induces serotonin N-acetyltransferase activity in photoreceptor-enriched retinal cell cultures. Involvement of calcium influx through l-type channels.

K(+)-evoked depolarization induces serotonin N-acetyltransferase activity in photoreceptor-enriched retinal cell cultures. Involvement of calcium influx through l-type channels.

Abstract：

:The roles of membrane depolarization and calcium influx in the regulation of retinal serotonin N-acetyltransferase (NAT) activity were investigated in low-density monolayer cultures of chick retinal cells, in which photoreceptors represented approximately 70% of the total cell population. NAT activity expressed by the cells in these cultures was markedly increased by elevating the concentration of extracellular K(+). Activity increased rapidly during the first 6 h of exposure to K(+), and remained elevated for at least 30 h. Chelation of calcium in the culture medium abolished the K(+)-evoked increase in NAT activity. Antagonists of voltage-sensitive calcium channels, nifedipine, methoxyverapamil (D600), Mn(2+), Mg(2+), and Cd(2+) inhibited the K(+)-evoked increase of NAT activity. Bay K 8644, a dihydropyridine calcium channel agonist, increased NAT activity when added alone and potentiated the K(+)-evoked increase of activity. The effect of Bay K 8644 was antagonized by nifedipine. Addition of nifedipine 18 h after addition of K(+), when NAT activity is elevated, caused activity to decrease to basal levels. These studies indicate that the increase of retinal NAT activity induced by K(+)-depolarization is mediated by a calcium-dependent process that involves sustained Ca(2+) influx through L-type voltage-sensitive Ca(2+)-channels.

journal_name

Neurochem Int

journal_title

Neurochemistry international

authors

Avendano G,Butler BJ,Michael Iuvone P

doi

10.1016/0197-0186(90)90075-5

subject

Has Abstract

pub_date

1990-01-01 00:00:00

pages

117-26

issue

1

eissn

0197-0186

issn

1872-9754

pii

0197-0186(90)90075-5

journal_volume

17

pub_type

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