Inhibition by ethanol of forskolin-stimulated adenylate cyclase in a murine neuroblastoma clone (N1E-115)

Scott Stenstrom; Marvin Seppala; Michael Pfenning; Elliott Richelson

doi:10.1016/0006-2952(85)90226-6

Inhibition by ethanol of forskolin-stimulated adenylate cyclase in a murine neuroblastoma clone (N1E-115)

Scott Stenstrom, Marvin Seppala, Michael Pfenning, Elliott Richelson

Neuroscience

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

Forskolin, a diterpene activator of adenylate cyclase, stimulated the formation of cyclic AMP in intact murine neuroblastoma clone N1E-115 cells and stimulated adenylate cyclase activity in a membranal preparation from these cells. Ethanol caused a concentration-dependent inhibition of the forskolin-stimulated responses in both preparations. In intact cells, the inhibition appeared to be noncompetitive. However, in the membranal preparation the inhibition was more of a competitive nature. In addition, there was also a large difference in the amount of inhibition in the two systems. Thus, the inhibition by ethanol was nearly twice as much with intact cells as with membranes. Sucrose appeared to mimic these effects of ethanol, suggesting that with intact cells the effect of this alcohol may be due, in part, to changes in cellular osmotic pressure.

Original language	English (US)
Pages (from-to)	3655-3659
Number of pages	5
Journal	Biochemical Pharmacology
Volume	34
Issue number	20
DOIs	https://doi.org/10.1016/0006-2952(85)90226-6
State	Published - Oct 15 1985

ASJC Scopus subject areas

Pharmacology

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title = "Inhibition by ethanol of forskolin-stimulated adenylate cyclase in a murine neuroblastoma clone (N1E-115)",

abstract = "Forskolin, a diterpene activator of adenylate cyclase, stimulated the formation of cyclic AMP in intact murine neuroblastoma clone N1E-115 cells and stimulated adenylate cyclase activity in a membranal preparation from these cells. Ethanol caused a concentration-dependent inhibition of the forskolin-stimulated responses in both preparations. In intact cells, the inhibition appeared to be noncompetitive. However, in the membranal preparation the inhibition was more of a competitive nature. In addition, there was also a large difference in the amount of inhibition in the two systems. Thus, the inhibition by ethanol was nearly twice as much with intact cells as with membranes. Sucrose appeared to mimic these effects of ethanol, suggesting that with intact cells the effect of this alcohol may be due, in part, to changes in cellular osmotic pressure.",

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T1 - Inhibition by ethanol of forskolin-stimulated adenylate cyclase in a murine neuroblastoma clone (N1E-115)

AU - Stenstrom, Scott

AU - Seppala, Marvin

AU - Pfenning, Michael

AU - Richelson, Elliott

PY - 1985/10/15

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N2 - Forskolin, a diterpene activator of adenylate cyclase, stimulated the formation of cyclic AMP in intact murine neuroblastoma clone N1E-115 cells and stimulated adenylate cyclase activity in a membranal preparation from these cells. Ethanol caused a concentration-dependent inhibition of the forskolin-stimulated responses in both preparations. In intact cells, the inhibition appeared to be noncompetitive. However, in the membranal preparation the inhibition was more of a competitive nature. In addition, there was also a large difference in the amount of inhibition in the two systems. Thus, the inhibition by ethanol was nearly twice as much with intact cells as with membranes. Sucrose appeared to mimic these effects of ethanol, suggesting that with intact cells the effect of this alcohol may be due, in part, to changes in cellular osmotic pressure.

AB - Forskolin, a diterpene activator of adenylate cyclase, stimulated the formation of cyclic AMP in intact murine neuroblastoma clone N1E-115 cells and stimulated adenylate cyclase activity in a membranal preparation from these cells. Ethanol caused a concentration-dependent inhibition of the forskolin-stimulated responses in both preparations. In intact cells, the inhibition appeared to be noncompetitive. However, in the membranal preparation the inhibition was more of a competitive nature. In addition, there was also a large difference in the amount of inhibition in the two systems. Thus, the inhibition by ethanol was nearly twice as much with intact cells as with membranes. Sucrose appeared to mimic these effects of ethanol, suggesting that with intact cells the effect of this alcohol may be due, in part, to changes in cellular osmotic pressure.

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