Nongenomic inhibition of catecholamine secretion by 17 beta-estradiol in PC12 cells
SCIE
SCOPUS
- Title
- Nongenomic inhibition of catecholamine secretion by 17 beta-estradiol in PC12 cells
- Authors
- Kim, YJ; Hur, EM; Park, TJ; Kim, KT
- Date Issued
- 2000-06
- Publisher
- LIPPINCOTT WILLIAMS & WILKINS
- Abstract
- We investigated the effects of 17 beta-estradiol, an estrogen, on [H-3]norepinephrine ([H-3]NE) secretion in PC12 cells. Pretreatment with 17 beta-estradiol reduced 70 mM K+-induced [H-3]NE secretion in a concentrationdependent manner with a half-maximal inhibitory concentration (IC50) of 2 +/- 1 mu M. The 70 mM K+-induced cytosolic free Ca2+ concentration ([Ca2+](i)) rise was also reduced when the cells were treated with 17 beta-estradiol (IC50 = 15 +/- 2 mu M). Studies with voltage-sensitive calcium channel (VSCC) antagonists such as nifedipine and omega-conotoxin GVIA revealed that both L- and N-type VSCCs were affected by 17 beta-estradiol treatment. The 17 beta-estradiol effect was not changed by pretreatment of the cells with actinomycin D and cycloheximide for 5 h. In addition, treatment with pertussis or cholera toxin did not affect the inhibitory effect of 17 beta-estradiol. 17 beta-Estradiol also inhibited the ATP-induced [H-3]NE secretion and [Ca2+](i) rise. In PC12 cells, the ATP-induced [Ca2+](i) rise is known to occur through P2X(2) receptors, the P2Y(2)-mediated phospholipase C (PLC) pathway, and VSCCs. 17 beta-Estradiol pretreatment during complete inhibition of the PLC pathway and VSCCs inhibited the ATP-induced [Ca2+](i) rise. Our results suggest that 17 beta-estradiol inhibits catecholamine secretion by inhibiting L- and N-type Ca2+ channels and P2X(2) receptors in a nongenomic manner.
- Keywords
- 17 beta-estradiol; catecholamine secretion; nongenomic inhibition; voltage-sensitive calcium channel; P2X(2) receptor; PC12 cell; VASCULAR SMOOTH-MUSCLE; SENSITIVE CALCIUM CHANNELS; STEROID-HORMONES; CA2+ CURRENTS; RECEPTORS; ESTRADIOL; RESPONSES; BINDING
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/20011
- DOI
- 10.1046/j.1471-4159.2000.0742490.x
- ISSN
- 0022-3042
- Article Type
- Article
- Citation
- JOURNAL OF NEUROCHEMISTRY, vol. 74, no. 6, page. 2490 - 2496, 2000-06
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