2009
DOI: 10.1586/ecp.09.6
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Emerging therapeutic targets for the treatment of nicotine addiction

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Cited by 6 publications
(2 citation statements)
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“…mGlu5-receptor blockade in the nucleus accumbens is effective in preventing relapse to drug seeking as well as neurochemical changes associated with drug reinstatement (Bespalov et al, 2005; Schroeder et al, 2008). mGlu5-receptor NAMs hold promise in the treatment of drug addiction, and AFQ056 is under clinical development for the treatment of tobacco smoking (Kenny, 2009). However, it should be highlighted that mGlu5-receptor blockade increases somatic signs and reward deficits associated with nicotine withdrawal (Liechti and Markou, 2006), suggesting that mGlu5-receptor NAMs should be associated with drugs that lower the reward threshold (e.g., bupropion) in the acute phase of nicotine withdrawal.…”
Section: Detailed Description Of Mglu Receptor Subtypesmentioning
confidence: 99%
“…mGlu5-receptor blockade in the nucleus accumbens is effective in preventing relapse to drug seeking as well as neurochemical changes associated with drug reinstatement (Bespalov et al, 2005; Schroeder et al, 2008). mGlu5-receptor NAMs hold promise in the treatment of drug addiction, and AFQ056 is under clinical development for the treatment of tobacco smoking (Kenny, 2009). However, it should be highlighted that mGlu5-receptor blockade increases somatic signs and reward deficits associated with nicotine withdrawal (Liechti and Markou, 2006), suggesting that mGlu5-receptor NAMs should be associated with drugs that lower the reward threshold (e.g., bupropion) in the acute phase of nicotine withdrawal.…”
Section: Detailed Description Of Mglu Receptor Subtypesmentioning
confidence: 99%
“…BDNF, which has been shown to be increased in the hippocampus following exercise (Fuss et al, ) and chronic nicotine treatment (Czubak et al, ; Kenny, ; Aydin et al, ), has also been shown to specifically up‐regulate the intracellular pool of α7‐, but not β2*‐, containing nAChRs in cultured hippocampal neurons (Zhou et al, ; Massey et al, ). As a result, we postulated that the observed exercise‐induced region‐specific up‐regulation of α7 nAChR in the brain of nicotine‐treated mice might be mediated by an elevation of BDNF levels.…”
Section: Discussionmentioning
confidence: 99%