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Alcohol Clin Exp Res. 2012 Mar;36(3):443-56. doi: 10.1111/j.1530-0277.2011.01631.x. Epub 2011 Oct 20.

Ethanol alters opioid regulation of Ca(2+) influx through L-type Ca(2+) channels in PC12 cells.

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1
Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California 92037, USA.

Abstract

BACKGROUND:

Studies at the behavioral and synaptic level show that effects of ethanol on the central nervous system can involve the opioid signaling system. These interactions may alter the function of a common downstream target. In this study, we examined Ca(2+) channel function as a potential downstream target of interactions between ethanol and μ or κ opioid receptor signaling.

METHODS:

The studies were carried out in a model system, undifferentiated PC12 cells transfected with μ or κ opioid receptors. The PC12 cells express L-type Ca(2+) channels, which were activated by K(+) depolarization. Ca(2+) imaging was used to measure relative Ca(2+) flux during K(+) depolarization and the modulation of Ca(2+) flux by opioids and ethanol.

RESULTS:

Ethanol, μ receptor activation, and κ receptor activation all reduced the amplitude of the Ca(2+) signal produced by K(+) depolarization. Pretreatment with ethanol or combined treatment with ethanol and μ or κ receptor agonists caused a reduction in the amplitude of the Ca(2+) signal that was comparable to or smaller than that observed for the individual drugs alone, indicating an interaction by the drugs at a downstream target (or targets) that limited the modulation of Ca(2+) flux through L-type Ca(2+) channels.

CONCLUSIONS:

These studies provide evidence for a cellular mechanism that could play an important role in ethanol regulation of synaptic transmission and behavior through interactions with the opioid signaling.

PMID:
22014285
PMCID:
PMC3266970
DOI:
10.1111/j.1530-0277.2011.01631.x
[Indexed for MEDLINE]
Free PMC Article
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