Plasma nicotine and cotinine concentrations in mice after chronic oral nicotine administration and challenge doses

Pekonen, Kirsi; Karlsson, Catarina; Laakso, Into; Ahtee, Liisa

doi:10.1016/0928-0987(93)90013-z

Cited by 46 publications

(47 citation statements)

References 20 publications

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“…In addition, increased nAChR binding was measured at plasma levels of nicotine that are within the range reported for smokers (10-50 ng ml -1 ; Benowitz and Jacob, 1984;Russell et al, 1980), and similar to those achieved in mice after long-term treatment with comparable doses of nicotine, administered either via osmotic minipumps (Metzger et al, 2007), constant i.v. infusion (Marks et al, 2004), or in the drinking water (Pekonen et al, 1993). The current experimental design thus resulted in blood plasma levels of nicotine that are physiologically relevant to the human condition.…”

Section: Discussionmentioning

confidence: 99%

Genetic deletion of the adenosine A2A receptor prevents nicotine-induced upregulation of α7, but not α4β2* nicotinic acetylcholine receptor binding in the brain

et al. 2013

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Section: Discussionmentioning

confidence: 99%

Genetic deletion of the adenosine A2A receptor prevents nicotine-induced upregulation of α7, but not α4β2* nicotinic acetylcholine receptor binding in the brain

et al. 2013

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“…We have shown that by increasing gradually the concentration, nicotine can be administered to mice in the drinking water at concentrations high enough to yield plasma nicotine concentrations clearly above those found in smokers (Pekonen et al 1993). In addition, in preliminary studies we also found that the 7-week administration of nicotine in the drinking water induces tolerance towards nicotine's hypothermia-producing effect and towards acute actions of nicotine on striatal DA metabolism (Pekonen et al 1991 and unpublished observations, Pietil~i K, Salmihen O, Leikola-Pelho T, Ahtee L).…”

Section: Introductionmentioning

confidence: 99%

Chronic oral nicotine administration affects the circadian rhythm of dopamine and 5-hydroxytryptamine metabolism in the striata of mice

Pietilä

Laakso

Ahtee

1995

Naunyn-Schmiedeberg's Arch Pharmacol

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The effect of chronic oral administration of nicotine on the circadian rhythm of striatal dopamine (DA) and 5-hydroxytryptamine (5-HT) was studied in mice. Mice receiving nicotine in their drinking water and control mice drinking tap water were killed at 05:00, 11:00, 15:00 or 21:00 hours on the 50th day of chronic administration. The plasma concentrations of nicotine and cotinine, as well the striatal concentrations of DA, 5-HT and their metabolites 3,4 dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT), homovanilic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were estimated. The largest plasma concentrations of nicotine and cotinine were found at 05:00, when they were more than double the concentrations found at the other times studied. This indicates that the mice, typically for nocturnal animals, consumed most of their daily drinking water at night. In the control mice, the striatal DA and 3-MT concentrations showed circadian variation and were lowest at 11:00. The 5-HIAA concentrations also varied, being highest at 11:00. In the nicotine-treated mice the circadian variations in striatal monoamines were altered and more pronounced than in the controls. The concentrations of DA, DOPAC, HVA and 5-HIAA were highest at 11:00 and that of 5-HT at 21:00. The striatal DA, DOPAC, HVA and 5-HIAA concentrations in the nicotine-treated mice were significantly higher at 11:00 and the 5-HT concentrations at 21:00 than in the control mice, and, in contrast to the control mice, in the mice treated with chronic nicotine no circadian rhythm was observed in the 3-MT. No elevation of striatal DA metabolites occurred in the nicotine-treated mice compared with the controls when the plasma nicotine concentration was at its peak at 05:00. This finding suggests development of tolerance to the nicotine-induced changes in striatal DA metabolism. Further, our findings suggest that the chronic administration of nicotine in the drinking water of mice alters the circadian pattern of striatal DA and, to a lesser extent, that of 5-HT, and thus may affect the functions regulated by these transmitters.

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“…Administration of nicotine in the drinking water is a less stressful alternative to repeated injection for chronic exposure experiments [20]. This method is very different from rapid infusion methods, such as smoking or jugular infusion, but results in intermittent exposure only during the waking period, and is sufficient to cause neuronal adaptations, including upregulation of nicotinic binding sites, that are observed in the brains of human smokers [18,19,26].…”

Section: Introductionmentioning

confidence: 99%

Voluntary oral nicotine intake in mice down-regulates GluR2 but does not modulate depression-like behaviors

Vieyra-Reyes¹,

Picciotto²,

Mineur³

2008

Neuroscience Letters

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Repeated exposure to nicotine induces adaptive changes in the central nervous system including the mesolimbic dopamine (DA) projections from the ventral tegmental area (VTA) to the nucleus accumbens (NAc). These modifications can modulate nicotine reward and reinforcement, but also anxiety and depression-related behaviors. The development of addiction-related phenotypes is known to be modulated by regulation of glutamate receptors, as well as activation of transcription factors including cAMP response element-binding protein (CREB), in the NAc.We investigated the effects of nicotine pre-exposure on nicotine preference and levels of Glur1/2 and CREB in the mesolimbic system in male mice C57BL/6J and BALB/c inbred mice. We also evaluated locomotor activity, anxiety-like and depression-like behaviors known to be affected by nicotine. There were few behavioral changes in mice subjected to chronic nicotine exposure, but there was a marked regulation of GluR2 in the mesolimbic system. Both treated and non-treated animals showed a significant preference for nicotine when facing a choice with a control solution.These results suggest that voluntary nicotine drinking induces nicotine preference in mice, but does not alter a number of affective behaviors. In addition, alterations in CREB and GluR1 levels are not sufficient to explain preference for nicotine in a 2-bottle choice paradigm.

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Plasma nicotine and cotinine concentrations in mice after chronic oral nicotine administration and challenge doses

Cited by 46 publications

References 20 publications

Genetic deletion of the adenosine A2A receptor prevents nicotine-induced upregulation of α7, but not α4β2* nicotinic acetylcholine receptor binding in the brain

Genetic deletion of the adenosine A2A receptor prevents nicotine-induced upregulation of α7, but not α4β2* nicotinic acetylcholine receptor binding in the brain

Chronic oral nicotine administration affects the circadian rhythm of dopamine and 5-hydroxytryptamine metabolism in the striata of mice

Voluntary oral nicotine intake in mice down-regulates GluR2 but does not modulate depression-like behaviors

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