1999
DOI: 10.1007/s11064-999-0001-1
|View full text |Cite
|
Sign up to set email alerts
|

The Effect of Cotinine on Nicotine- and Cocaine-Induced Dopamine Release in the Nucleus Accumbens

Abstract: Cotinine is the major metabolite of nicotine. Nicotine is rapidly metabolized and has a short half-life, but cotinine is metabolized and eliminated at a much lower rate. Because of the resulting increase with time in the cotinine to nicotine ratio in the body, including in the brain, it is of interest to examine the effect of cotinine on nicotine-induced changes. In studies on conscious, freely-moving rats, intravenous administration of either nicotine or cocaine induced the release of dopamine in the nucleus … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
11
0

Year Published

2004
2004
2022
2022

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 18 publications
(11 citation statements)
references
References 29 publications
0
11
0
Order By: Relevance
“…Ki values for displacing [ 3 H]cytisine binding (presumably high-affinity α4β2 * subtype; the * denotes other nAChR subunits) were over 200 µM for cotinine and 0.6 nM for nicotine (Anderson and Arneric, 1994). Consistently, cotinine up to 1 µM produced minimal effect on [ 3 H]cytisine binding, whereas nicotine induced over 70% inhibition of [ 3 H]cytisine binding in rat cerebral cortex preparations (Sziraki et al, 1999). Cotinine and nicotine were reported to display equal efficacy in displacing [ 125 I]α-bungarotoxin binding (presumably lowaffinity α7 nAChRs), but cotinine was ∼100 fold less potent than nicotine, with IC 50 values at 1 mM and 10 µM, respectively (Riah et al, 1999).…”
Section: Pharmacodynamics Of Cotininementioning
confidence: 86%
“…Ki values for displacing [ 3 H]cytisine binding (presumably high-affinity α4β2 * subtype; the * denotes other nAChR subunits) were over 200 µM for cotinine and 0.6 nM for nicotine (Anderson and Arneric, 1994). Consistently, cotinine up to 1 µM produced minimal effect on [ 3 H]cytisine binding, whereas nicotine induced over 70% inhibition of [ 3 H]cytisine binding in rat cerebral cortex preparations (Sziraki et al, 1999). Cotinine and nicotine were reported to display equal efficacy in displacing [ 125 I]α-bungarotoxin binding (presumably lowaffinity α7 nAChRs), but cotinine was ∼100 fold less potent than nicotine, with IC 50 values at 1 mM and 10 µM, respectively (Riah et al, 1999).…”
Section: Pharmacodynamics Of Cotininementioning
confidence: 86%
“…Further, cotinine binds to nicotinic receptors, although at a substantially lower potency and lower affinity than nicotine (Anderson and Arneric, 1994; O’Leary et al, 2008; Sloan et al, 1984; Vainio and Tuominen, 2001). Interestingly, cotinine also inhibits nicotine-induced dopamine release in the NAc in adult rats (Sziraki et al, 1999). Thus, cotinine appears to act as a partial agonist at nicotinic receptors in the mesolimbic system.…”
Section: Discussionmentioning
confidence: 99%
“…These studies suggest that cotinine is much less potent than nicotine in binding to nAChRs. Furthermore, cotinine at physiological concentrations (0.1-1µM) did not inhibit 3 Hcytisine binding (Sziraki et al 1999). Cotinine at 10µM had no agonistic or antagonistic activity on α4β2* or α7 nAChRs (Terry et al 2015).…”
Section: Downloaded Frommentioning
confidence: 91%