Abstract
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 (-)-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 5-123I-iodo-A-85380 ( 123I-5IA) SPECT on nonsmokers and smokers (n = 16) who had quit smoking for 4 h, 10 d, and 21 d and calculated and compared distribution volumes (Vt) of 123I-5IA. Results: The binding potential of nAChRs (Vt of 123I-5IA) in the brains of smokers decreased by 33.5% ± 10.5% after 4 h of smoking cessation, increased by 25.7% ± 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.
| Original language | English |
|---|---|
| Pages (from-to) | 1829-1835 |
| Number of pages | 7 |
| Journal | Journal of Nuclear Medicine |
| Volume | 48 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - Nov 1 2007 |
| Externally published | Yes |
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Keywords
- I-5IA
- Human brain
- Nicotinic acetylcholine receptors
- Quantitative measurement
- Smoking withdrawal
- SPECT
ASJC Scopus subject areas
- Radiological and Ultrasound Technology
Cite this
Temporal change in human nicotinic acetylcholine receptor after smoking cessation : 5IA SPECT study. / Mamede, Marcelo; Ishizu, Koichi; Ueda, Masashi; Mukai, Takahiro; Iida, Yasuhiko; Kawashima, Hidekazu; Fukuyama, Hidenao; Togashi, Kaori; Saji, Hideo.
In: Journal of Nuclear Medicine, Vol. 48, No. 11, 01.11.2007, p. 1829-1835.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Temporal change in human nicotinic acetylcholine receptor after smoking cessation
T2 - 5IA SPECT study
AU - Mamede, Marcelo
AU - Ishizu, Koichi
AU - Ueda, Masashi
AU - Mukai, Takahiro
AU - Iida, Yasuhiko
AU - Kawashima, Hidekazu
AU - Fukuyama, Hidenao
AU - Togashi, Kaori
AU - Saji, Hideo
PY - 2007/11/1
Y1 - 2007/11/1
N2 - 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 (-)-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 5-123I-iodo-A-85380 ( 123I-5IA) SPECT on nonsmokers and smokers (n = 16) who had quit smoking for 4 h, 10 d, and 21 d and calculated and compared distribution volumes (Vt) of 123I-5IA. Results: The binding potential of nAChRs (Vt of 123I-5IA) in the brains of smokers decreased by 33.5% ± 10.5% after 4 h of smoking cessation, increased by 25.7% ± 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.
AB - 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 (-)-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 5-123I-iodo-A-85380 ( 123I-5IA) SPECT on nonsmokers and smokers (n = 16) who had quit smoking for 4 h, 10 d, and 21 d and calculated and compared distribution volumes (Vt) of 123I-5IA. Results: The binding potential of nAChRs (Vt of 123I-5IA) in the brains of smokers decreased by 33.5% ± 10.5% after 4 h of smoking cessation, increased by 25.7% ± 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.
KW - I-5IA
KW - Human brain
KW - Nicotinic acetylcholine receptors
KW - Quantitative measurement
KW - Smoking withdrawal
KW - SPECT
UR - http://www.scopus.com/inward/record.url?scp=36049038636&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=36049038636&partnerID=8YFLogxK
U2 - 10.2967/jnumed.107.043471
DO - 10.2967/jnumed.107.043471
M3 - Article
C2 - 17942810
AN - SCOPUS:36049038636
VL - 48
SP - 1829
EP - 1835
JO - Journal of Nuclear Medicine
JF - Journal of Nuclear Medicine
SN - 0161-5505
IS - 11
ER -