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Effects of ethanol on phosphoinositide hydrolysis and muscarinic acetylcholine receptor number in SH-SY5Y cells

Caron, Murielle ; Andersson, Amelie LU and Alling, Christer LU (2000) In Life Sciences 67(4). p.56-447
Abstract

Previous studies suggest that the effects of ethanol on carbachol-stimulated I(1,4,5)P3 formation and on the number of mAChRs may be independent of each other. The aim of this work was to further study this hypothesis. Human neuroblastoma SH-SY5Y cells were used as a model system. Acute exposure of the cells to 100 mM ethanol induced a decrease in [3H]N-methylscopolamine ([3H]NMS) binding at 30 seconds which was of lower magnitude and of shorter duration than the previously described ethanol-induced inhibition of the peak of carbachol-stimulated I(1,4,5)P3 formation. Long-term ethanol treatment of the cells induced a time- and concentration-dependent increase in [3H]NMS binding. Three hours of 100 mM ethanol treatment were sufficient to... (More)

Previous studies suggest that the effects of ethanol on carbachol-stimulated I(1,4,5)P3 formation and on the number of mAChRs may be independent of each other. The aim of this work was to further study this hypothesis. Human neuroblastoma SH-SY5Y cells were used as a model system. Acute exposure of the cells to 100 mM ethanol induced a decrease in [3H]N-methylscopolamine ([3H]NMS) binding at 30 seconds which was of lower magnitude and of shorter duration than the previously described ethanol-induced inhibition of the peak of carbachol-stimulated I(1,4,5)P3 formation. Long-term ethanol treatment of the cells induced a time- and concentration-dependent increase in [3H]NMS binding. Three hours of 100 mM ethanol treatment were sufficient to increase the number of mAChRs at the cell surface but these receptors were not immediately functionally active, suggesting that they may be newly synthesized. Furthermore, the ethanol-induced potentiation of carbachol-stimulated I(1,4,5)P3 formation, after two days, was, for all ethanol concentrations tested, of higher magnitude than the ethanol-induced increase in mAChR number. Together, these data indicate that both acute and chronic ethanol-induced changes in carbachol-stimulated I(1,4,5)P3 formation may not only be explained by changes in mAChR density at the cell surface but may rather be the consequence of actions of ethanol down-stream of the receptor.

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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Binding Sites/drug effects, Carbachol/pharmacology, Dose-Response Relationship, Drug, Ethanol/pharmacology, Humans, Hydrolysis, N-Methylscopolamine/metabolism, Neuroblastoma/metabolism, Phosphatidylinositols/metabolism, Receptors, Muscarinic/metabolism, Tumor Cells, Cultured/drug effects
in
Life Sciences
volume
67
issue
4
pages
56 - 447
publisher
Elsevier
external identifiers
  • scopus:0034674792
  • pmid:11003054
ISSN
0024-3205
DOI
10.1016/s0024-3205(00)00641-x
language
English
LU publication?
yes
id
94203ee7-57a8-4fc0-8c62-f8e774d8a0ad
date added to LUP
2021-05-27 17:10:05
date last changed
2022-02-01 22:01:13
@article{94203ee7-57a8-4fc0-8c62-f8e774d8a0ad,
  abstract     = {{<p>Previous studies suggest that the effects of ethanol on carbachol-stimulated I(1,4,5)P3 formation and on the number of mAChRs may be independent of each other. The aim of this work was to further study this hypothesis. Human neuroblastoma SH-SY5Y cells were used as a model system. Acute exposure of the cells to 100 mM ethanol induced a decrease in [3H]N-methylscopolamine ([3H]NMS) binding at 30 seconds which was of lower magnitude and of shorter duration than the previously described ethanol-induced inhibition of the peak of carbachol-stimulated I(1,4,5)P3 formation. Long-term ethanol treatment of the cells induced a time- and concentration-dependent increase in [3H]NMS binding. Three hours of 100 mM ethanol treatment were sufficient to increase the number of mAChRs at the cell surface but these receptors were not immediately functionally active, suggesting that they may be newly synthesized. Furthermore, the ethanol-induced potentiation of carbachol-stimulated I(1,4,5)P3 formation, after two days, was, for all ethanol concentrations tested, of higher magnitude than the ethanol-induced increase in mAChR number. Together, these data indicate that both acute and chronic ethanol-induced changes in carbachol-stimulated I(1,4,5)P3 formation may not only be explained by changes in mAChR density at the cell surface but may rather be the consequence of actions of ethanol down-stream of the receptor.</p>}},
  author       = {{Caron, Murielle and Andersson, Amelie and Alling, Christer}},
  issn         = {{0024-3205}},
  keywords     = {{Binding Sites/drug effects; Carbachol/pharmacology; Dose-Response Relationship, Drug; Ethanol/pharmacology; Humans; Hydrolysis; N-Methylscopolamine/metabolism; Neuroblastoma/metabolism; Phosphatidylinositols/metabolism; Receptors, Muscarinic/metabolism; Tumor Cells, Cultured/drug effects}},
  language     = {{eng}},
  number       = {{4}},
  pages        = {{56--447}},
  publisher    = {{Elsevier}},
  series       = {{Life Sciences}},
  title        = {{Effects of ethanol on phosphoinositide hydrolysis and muscarinic acetylcholine receptor number in SH-SY5Y cells}},
  url          = {{http://dx.doi.org/10.1016/s0024-3205(00)00641-x}},
  doi          = {{10.1016/s0024-3205(00)00641-x}},
  volume       = {{67}},
  year         = {{2000}},
}