Modulation of Nicotine Receptors by Chronic Exposure to Nicotinic Agonists and Antagonists

Collins, Allan C.; Bhat, Ratan V.; Pauly, James R.; Marks, Michael J.

doi:10.1002/9780470513965.ch5

Cited by 38 publications

(11 citation statements)

References 21 publications

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“…In the present study, the interval of 21 d was thought to be the recovery time during which upregulated nAChRs return to the level of the nonsmoker. This suggests that nicotineinduced upregulation of receptor number is a temporary effect, similar to that found in rodents (28,29).…”

Section: Discussionsupporting

confidence: 54%

Temporal Change in Human Nicotinic Acetylcholine Receptor After Smoking Cessation: 5IA SPECT Study

Mamede¹,

Ishizu²,

Ueda³

et al. 2007

Journal of Nuclear Medicine

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Nicotinic acetylcholine receptors (nAChRs) are of great interest because they are implicated in various brain functions. They also are thought to play an important role in nicotine addiction of smokers. Chronic (2)-nicotine, a nAChR agonist, treatment in mice and rats elicits a dose-dependent increase in nAChRs in the brain. Upregulation of nAChRs in postmortem human brains of smokers has also been reported. However, changes in nAChRs after cigarette smoking cessation in humans are poorly understood. The aim of this study was to detect the dynamic changes of nAChRs after smoking and smoking cessation in the brains of living subjects. Methods: We performed 5-123 Iiodo-A-85380 ( 123 I-5IA) SPECT on nonsmokers and smokers (n 5 16) who had quit smoking for 4 h, 10 d, and 21 d and calculated and compared distribution volumes (Vt) of 123 I-5IA. Results: The binding potential of nAChRs (Vt of 123 I-5IA) in the brains of smokers decreased by 33.5% 6 10.5% after 4 h of smoking cessation, increased by 25.7% 6 9.2% after 10 d of smoking cessation, and decreased to the level of nonsmokers after 21 d of smoking cessation. Conclusion: Because the upregulation of the nAChRs of the smokers after chronic exposure of the nicotine was downregulated to the nonsmokers' level by around 21 d after smoking cessation, the upregulation is a temporary effect. The decrease in nicotinic receptors to nonsmoker levels may be the breaking point during the nicotine withdrawal period.

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Section: Discussionsupporting

confidence: 54%

Temporal Change in Human Nicotinic Acetylcholine Receptor After Smoking Cessation: 5IA SPECT Study

Mamede¹,

Ishizu²,

Ueda³

et al. 2007

Journal of Nuclear Medicine

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“…Disruption of glucocorticoid synthesis or blockade of CRF receptors suppresses stimulant self-administration (Goeders, 2002). Glucocorticoids may attenuate CNS sensitivity to nicotine (Caggiula et al, 1998;Collins et al, 1990), leading to a withdrawal-like state under conditions of high stress. On the other hand, longterm exposure to nicotine may lead to alterations in the stress response, providing a possible mechanism through which stress increases craving and risk for relapse.…”

Section: Discussion and Proposed Modelmentioning

confidence: 98%

“…6). This model is based on studies reviewed above and builds on research models with other drugs of addiction, indicating that drug deprivation and stress may produce strong motivational states leading to reinstatement of drug administration (Buczek et al, 1999;Epping-Jordan et al, 1998;Koob and Le Moal, 1997;Collins et al, 1990).…”

Section: Discussion and Proposed Modelmentioning

confidence: 99%

Hypothalamic–Pituitary–Adrenocortical responses to psychological stress and risk for smoking relapse

Al’Absi

2006

International Journal of Psychophysiology

144

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“…This was based on a minimum period of five half-lives (galantamine plasma half-life ∼7 h; Lilienfeld 2002) to ensure significant clearance based on pharmacokinetics. Furthermore, a 3-day washout period was also selected based on animal studies showing that nicotinic agonists (including nicotine) can induce upregulation of nAChRs, with receptor density returning to control levels within 7-10 days in mice ([ 3 H]-nicotine binding; Marks et al 1985) and 15-20 days in rats ([ 3 H]-cytisine binding; Koylu et al 1997) after cessation of treatment (for review, see Collins et al 1990). Therefore, the 3-day washout period not only ensured significant clearance of galantamine but also made it unlikely that receptor density would return to baseline levels before the post-treatment PET scan.…”

Section: Discussionmentioning

confidence: 99%

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

et al. 2008

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Performance on global measures of cognition significantly improved following galantamine treatment (p < 0.05). This improvement extended to specific cognitive measures of language and verbal learning. No significant differences in nAChR DV(S) before and after galantamine treatment were found. The treatment-induced improvement in cognition was not correlated with regional or global nAChR DV(S), suggesting that changes in nAChRs may not be responsible for the improvements in cognition following galantamine in patients with mild AD.

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Modulation of Nicotine Receptors by Chronic Exposure to Nicotinic Agonists and Antagonists

Cited by 38 publications

References 21 publications

Temporal Change in Human Nicotinic Acetylcholine Receptor After Smoking Cessation: 5IA SPECT Study

Temporal Change in Human Nicotinic Acetylcholine Receptor After Smoking Cessation: 5IA SPECT Study

Hypothalamic–Pituitary–Adrenocortical responses to psychological stress and risk for smoking relapse

Galantamine-induced improvements in cognitive function are not related to alterations in α4β2 nicotinic receptors in early Alzheimer’s disease as measured in vivo by 2-[18F]Fluoro-A-85380 PET

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