Pharmacological modulation of the α7 nicotinic acetylcholine receptor in a mouse model of mecamylamine-precipitated nicotine withdrawal

Jackson, Asti; Papke, Roger L.; Damaj, M. Imad

doi:10.1007/s00213-018-4879-7

Cited by 15 publications

(18 citation statements)

References 36 publications

(49 reference statements)

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“…In this study, it was found that NS1738 has three theoretical binding sites (Kuang et al, 2016). In a mouse in vivo study, this compound successfully blocked somatic behavioral signs of antagonist-precipitated nicotine withdrawal (Jackson et al, 2018). However, NS1738 did not block increased anxiety-related behaviors in the same mice (Jackson et al, 2018).…”

Section: Uci-30002mentioning

confidence: 82%

“…In a mouse in vivo study, this compound successfully blocked somatic behavioral signs of antagonist-precipitated nicotine withdrawal (Jackson et al, 2018). However, NS1738 did not block increased anxiety-related behaviors in the same mice (Jackson et al, 2018). Meanwhile, in the same study, the a7 nAChR orthosteric agonist PNU282986 significantly reduced both the somatic signs and anxiety-related behavior associated with antagonistprecipitated nicotine withdrawal.…”

Section: Uci-30002mentioning

confidence: 90%

“…In mice, PNU-120596 enhanced the hypothermic effects of nicotine (Moerke et al, 2016). In a different study, this compound blocked some of the behavioral effects associated with nicotine withdrawal in mice (Jackson et al, 2018). However, PNU-120596 did not block increased anxietyrelated behaviors in the same mice (Jackson et al, 2018).…”

Section: Uci-30002mentioning

confidence: 92%

“…There is also evidence that this receptor subtype plays some role in the reinforcing effects of nicotine, as rats self-administered significantly less nicotine after administration of an antagonist that prevented nicotine from interacting with a7-containing nAChRs (Markou and Paterson, 2001) despite evidence that a7 knockout mice self-administer nicotine to the same extent as controls (Pons et al, 2008). Furthermore, modulation of dopamine signaling by a7-containing nAChRs may also play a role in tobacco use disorder (Kaiser and Wonnacott, 2000), and additional studies indicate that a7-containing nAChRs may be important in the somatic signs of nicotine withdrawal (Jackson et al, 2018). Despite this, a7 nAChRs do not appear to be necessary for the nicotine discriminative stimulus, as a7 knockout mice can be readily trained to discriminate nicotine from saline (Stolerman et al, 2004).…”

Section: A Receptor Pharmacologymentioning

confidence: 99%

“…Yes Enhances the hypothermic effects of nicotine; blocks behavioral signs of nicotine withdrawal in mice; does not potentiate the effect of nicotine in the mouse drug discrimination assay Hurst et al, 2005;Barron et al, 2009;Moerke et al, 2016;Jackson et al, 2018 TQS Selective type II activity at a7 Yes N. A. Gronlien et al, 2007;Thomsen and Mikkelsen, 2012 A-867744 Selective type II activity at a7 Yes N. A.…”

Section: Uci-30002mentioning

confidence: 99%

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More than Smoke and Patches: The Quest for Pharmacotherapies to Treat Tobacco Use Disorder

2020

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Section: Uci-30002mentioning

confidence: 82%

Section: Uci-30002mentioning

confidence: 90%

Section: Uci-30002mentioning

confidence: 92%

Section: A Receptor Pharmacologymentioning

confidence: 99%

Section: Uci-30002mentioning

confidence: 99%

See 3 more Smart Citations

More than Smoke and Patches: The Quest for Pharmacotherapies to Treat Tobacco Use Disorder

2020

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The role of pituitary adenylyl cyclase activating polypeptide in affective signs of nicotine withdrawal

Nega

Marquez

Hamid

et al. 2020

J of Neuroscience Research

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Recent evidence implicates endogenous pituitary adenylyl cyclase activating polypeptide (PACAP) in the aversive effect of nicotine. In the present study, we assessed if nicotine-induced conditioned place preference (CPP) or affective signs of nicotine withdrawal would be altered in the absence of PACAP and if there were any sexrelated differences in these responses. Male and female mice lacking PACAP and their wild-type controls were tested for baseline place preference on day 1, received conditioning with saline or nicotine (1 mg/kg) on alternate days for 6 days and were then tested for CPP the next day. Mice were then exposed to four additional conditioning and were tested again for nicotine-induced CPP 24 hr later. Controls were conditioned with saline in both chambers and tested similarly. All mice were then, 96 hr later, challenged with mecamylamine (3 mg/kg), and tested for anxiety-like behaviors 30 min later. Mice were then, 2 hr later, forced to swim for 15 min and then tested for depression-like behaviors 24 hr later. Our results showed that male but not female mice lacking PACAP expressed a significant CPP that was comparable to their wild-type controls. In contrast, male but not female mice lacking PACAP exhibited reduced anxiety-and depression-like behaviors compared to their wild-type controls following the mecamylamine challenge. These results suggest that endogenous PACAP is involved in affective signs of nicotine withdrawal, but there is a sex-related difference in this response.

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Impact of modulation of the α7 nicotinic acetylcholine receptor on nicotine reward in the mouse conditioned place preference test

et al. 2019

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Rationale The α7 nicotinic acetylcholine receptor (nAChR) has been implicated as a target in modulating nicotine reward. However, the effect of pharmacological agents that have been shown to alter the channel properties of the α7 nAChR is not well understood in nicotine reward. Objectives This study aimed to investigate the impact of α7 nAChR pharmacological modulation on nicotine conditioned place preference (CPP) in mice by using positive allosteric modulators (PAMs) and a silent agonist. Methods The effect of the orthosteric α7 nAChR full agonist PNU282987 (1.3 and 9 mg/kg, s.c.), Type I α7 PAM NS1738 (1 and 10 mg/kg; i.p.), the Type II α7 PAM PNU120596 (0.3, 1, and 3 mg/kg, i.p.), and the α7 silent agonist NS6740 (1 and 3 mg/kg, i.p) on nicotine CPP was measured in mice. Mice were conditioned with either saline or nicotine (0.5 mg/kg) for 3 days in the CPP paradigm. Results The α7 full orthosteric agonist PNU282987 and the Type II α7 nAChR PAM PNU120596 reduced nicotine CPP, while the silent agonist NS6740 and Type I PAM NS1738 had no effect. The effects of PNU282987 and PNU120596 did not have an effect on morphine CPP. Conclusions Taken together, our results suggest that modulation of the α7 nAChR can play important roles in nicotine CPP in mice. In addition, the Type II α7 nAChR PAM PNU120596 attenuated nicotine reward suggesting that endogenous acetylcholine/choline tone is sufficient to reduce nicotine CPP. These findings highlight a beneficial effect of using α7 nAChR PAMs in nicotine reward.

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Pharmacological modulation of the α7 nicotinic acetylcholine receptor in a mouse model of mecamylamine-precipitated nicotine withdrawal

Cited by 15 publications

References 36 publications

More than Smoke and Patches: The Quest for Pharmacotherapies to Treat Tobacco Use Disorder

More than Smoke and Patches: The Quest for Pharmacotherapies to Treat Tobacco Use Disorder

The role of pituitary adenylyl cyclase activating polypeptide in affective signs of nicotine withdrawal

Impact of modulation of the α7 nicotinic acetylcholine receptor on nicotine reward in the mouse conditioned place preference test

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