Myers P R
J Cell Physiol. 1979 Jan;98(1):11-6. doi: 10.1002/jcp.1040980103.
PGE1 elicited a slow, dose-dependent membrane depolarization with an increase in membrane conductance in the somatic cell hybrid TCX11. The ED50 was 1-2 X 10(-8) M with maximal responses at 1-5 X 10(-7) M. Dopamine (DA) reversed the effect of PGE1 and caused the membrane potential and resistance to return to control levels. Chronic exposure of cells (measured in minutes) to DA alone would not cause this hyperpolarization. 5-HT was also tested and failed to consistently reverse the PGE1 effects. Chlorpromazine antagonized the effects of DA on the PGE1 response. The electrophysiological results reported here using TCX11 cells are discussed in light of previously reported biochemical results describing interactions of PGE1 and DA, and the electrophysiological effects of DA alone.
前列腺素E1（PGE1）在体细胞杂交瘤TCX11中引起缓慢的、剂量依赖性的膜去极化，并伴有膜电导增加。半数有效剂量（ED50）为1 - 2×10⁻⁸M，在1 - 5×10⁻⁷M时出现最大反应。多巴胺（DA）可逆转PGE1的作用，使膜电位和电阻恢复到对照水平。仅将细胞长期暴露于DA（以分钟计）不会引起这种超极化。5-羟色胺（5-HT）也经过测试，但未能始终如一地逆转PGE1的作用。氯丙嗪可拮抗DA对PGE1反应的影响。本文报道的使用TCX11细胞的电生理结果，结合先前报道的描述PGE1与DA相互作用的生化结果以及单独DA的电生理效应进行了讨论。
