Tobacco dependence is a chronic relapsing disorder and nicotine, the primary alkaloid in tobacco, acts at nicotinic receptors to stimulate dopamine release in brain, which is responsible for the reinforcing properties of nicotine, leading to addiction. Although the majority of tobacco users express the desire to quit, only a small percentage of those attempting to quit are successful using the currently available pharmacotherapies. Nicotine upregulates the number of specific nicotinic receptors on the neuronal cell surface. An increase in receptor trafficking or preferential stoichiometric assembly of receptor subunits involves changes in assembly, endoplasmic reticulum export, vesicle transport, decreased degradation, desensitization, enhanced maturation of functional pentamers, and pharmacological chaperoning. Understanding these changes on a mechanistic level is important to the development of nicotinic receptors as drug targets. For this reason, cutting-edge methodologies are being developed and employed to pinpoint distinct changes in localization, assembly, export, vesicle trafficking, and stoichiometry in order to further understand the physiology of these receptors and to evaluate the action of novel therapeutics for smoking cessation.
|Title of host publication||Neuromethods|
|Number of pages||14|
|State||Published - 2016|
Bibliographical noteFunding Information:
This research was supported by NIH grants DA03881, DA16176, and TR000117.
© Springer Science+Business Media New York 2016.
- Alpha4beta2 nicotinic receptors
- Nicotine addiction
- Receptor assembly
- Superecliptic pHluorin
- Tobacco-use cessation
- Total internal reflection fluorescence
ASJC Scopus subject areas
- Neuroscience (all)
- Biochemistry, Genetics and Molecular Biology (all)
- Pharmacology, Toxicology and Pharmaceutics (all)
- Psychiatry and Mental health