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Nicotine-induced increase in neuronal nicotinic receptors results from a decrease in the rate of receptor turnover

X Peng¹, V Gerzanich, R Anand

¹Department of Neuroscience, University of Pennsylvania Medical School, Philadelphia 19104-6074.

Molecular Pharmacology

|September 1, 1994

Summary

Chronic nicotine exposure increases brain nicotinic receptors. This up-regulation is a property of the alpha 4 beta 2 receptor protein itself, not a unique neuronal adaptation.

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Area of Science:

Neuroscience
Pharmacology
Molecular Biology

Background:

Chronic nicotine exposure elevates brain nicotine binding sites.
This increase is hypothesized as a neuronal adaptation to desensitized receptors.

Purpose of the Study:

To investigate if nicotine-induced receptor up-regulation is an intrinsic property of the alpha 4 beta 2 nicotinic acetylcholine receptor protein.
To determine if this up-regulation occurs independently of neuronal-specific adaptive mechanisms.

Main Methods:

Expressed alpha 4 beta 2 nicotinic acetylcholine receptors in Xenopus oocytes and a transfected fibroblast cell line.
Exposed these cells to chronic nicotine or other agonists.
Investigated the role of ion channel activity and receptor conformation in up-regulation using mecamylamine.

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Main Results:

Chronic nicotine exposure increased the amount of alpha 4 beta 2 receptors in cell lines.
The concentration dependence, time course, and extent of up-regulation mirrored findings in the brain.
Up-regulation occurred independently of ion flow and was also induced by mecamylamine, suggesting a conformational change.

Conclusions:

Nicotine-induced receptor up-regulation is an intrinsic property of the alpha 4 beta 2 nicotinic acetylcholine receptor protein.
This phenomenon does not require neuronal-specific adaptive responses.
Ligand binding induces a conformation that slows receptor degradation, leading to increased surface expression.