When positron emission tomography (PET) using a specific ligand for alpha 4 beta 2* (*other subunits may be present) nicotinic acetylcholine receptors was used to measure receptor occupancy, it was found that just 1 puff on a cigarette produced 50% occupancy and smoking a full cigarette more than 88% receptor occupancy. Desensitized nicotinic acetylcholine receptors have a higher affinity for acetylcholine than those in the state than can be activated. Nicotine upreguates nicotine binding sites and during nicotine withdrawal in humans, there is an increase in beta 2 nicotinic acetylcholine receptors. Since smokers maintain high nicotine blood levels throughout the day, this may be an attempt to maintain high occupancy and desensitization.
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Human Smoking Abstinence and Beta2 Nicotinic Ach Receptors
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CURRENT LESSON OBJECTIVES
- Describe the Sequence of Factors that leads to Smoking Addiction
- What is the mechanism by which nicotine produces its biological and behavioral effects?
- How do nicotinic acetylcholine receptor subtypes regulate dopamine release?
- How could nicotine alter tonic and phasic DA release to increase cue salience?
- What is an important pathway that inhibits nicotine intake?
- Why would smokers try to keep Beta 2 nicotinic receptors in a desensitized state?
- What is the role of corticotrophin-releasing factor (CRF) in nicotine withdrawal?
- What is the role of the insula cortex in drug seeking.
- How do nicotine and alcohol interact?
- Could monoamine oxidase inhibition play a role in the effects of smoking?
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