Antidepressants and Smoking Cessation

Gambassi, Giovanni; Bernabei, Roberto

doi:10.1001/archinte.159.11.1257

Cited by 7 publications

(2 citation statements)

References 20 publications

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“…This substance activates neurons, especially in the limbic system and the hippocampus. 47 Moreover, it increases mesocorticolimbic activity in the nucleus accumbens and prefrontal cortex. 48 In a smoker’s brain, the activity of monoamine oxidases (MAOs) is reduced (MAO B by approximately 40% and MAO A by approximately 28%), 49 which significantly reduces DA metabolism and is responsible for the neuroprotective effect, as it reduces smokers’ proneness to neuroleptic-induced Parkinsonism.…”

Section: Discussionmentioning

confidence: 99%

Neuroleptics and enrichment environment treatment in memory disorders and other central nervous system function observed in prenatally stressed rats

et al. 2014

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It is believed that the most effective method of treatment in schizophrenia is pharmacotherapy, in particular, the use of atypical neuroleptics like aripiprazole (ARI) and olanzapine (OLA). Moreover, studies of many authors have shown that enriched living conditions and tobacco smoke exposure can also affect the cognitive functions that are disturbed in the course of schizophrenia. The aim of the study was to find whether tobacco smoke and enrichment living conditions have the influence on cognitive functions in the newborn offspring of prenatally stressed rats and whether drugs such as ARI (1.5 mg/kg intraperitoneally (i.p.)) and OLA (0.5 mg/kg ip) in single and chronic treatment modify those functions (Morris water maze). The study (in the same conditions) also analyses immobility time (Porsolt test) and motor activity of animals that received ARI and OLA. It has been shown that ARI and OLA as well as enriched environment reduce cognitive function disorders and modify cognitive functions in rats exposed to tobacco smoke. In turn, current research has shown that nicotine has increased cognitive function disorders compared to the previous study (animals without tobacco smoke exposure).

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Section: Discussionmentioning

confidence: 99%

Neuroleptics and enrichment environment treatment in memory disorders and other central nervous system function observed in prenatally stressed rats

et al. 2014

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“…Similar results have been obtained by other authors, 44 Á 46 whereas Levin Á/ analysing acute NIC exposure Á/ reports improvement in working memory but not in reference memory. 47 NIC is known to activate neurones in some brain areas, eg, in the limbic system, that are crucial for neurocognitive processes, 29 and in both animals and humans hippocampus is known to play a key role in memorizing. After bilateral removal of the hippocampus the animals had more difficulty in reaching the immersed platform in the Morris test as compared to the rats with intact hippocampus, 48 whereas both groups of rats could easily locate the platform when it was not immersed.…”

Section: Daysmentioning

confidence: 99%

The influence of tobacco smoke and nicotine on antidepressant and memory-improving effects of venlafaxine

Nowakowska

Kus²,

Florek

et al. 2006

Hum Exp Toxicol

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In experimental and clinical studies, central nicotinic systems have been shown to play an important role in cognitive function. Nicotinic acetylcholine receptors also mediate the reinforcing properties of nicotine (NIC) in tobacco products. A variety of studies have shown that acute treatment with NIC or nicotinic agonists can improve working memory function. Moreover, it is known that the monoaminergic system plays an important role in memory function. And there is evidence suggesting that prolonged use of NIC may exert antidepressant action via nicotinic receptors. The purpose of this study was to investigate the interactions between a novel antidepressant, venlafaxine (VEN), a blocker of noradrenaline and 5–hydroxytryptamine reuptake sites, and pure NIC in the context of antidepressant and memory function in tobacco smoke exposed and nonexposed rats. The animals were subjected to Porsolt's test for testing antidepressant activity and their memory function (spatial memory) was evaluated in the Morris Water Maze Test. In tobacco smoke non–exposed and exposed rats both single and chronic administration of VEN (20 mg/kg po) shortened immobility time. NIC (0.2 mg/kg sc) significantly reduced immobility time on the 1st, 7th and 14th test days in both non–exposed and exposed rats. Combined VEN–NIC treatment in tobacco smoke non–exposed rats reduced immobility too. This effect of the combination of drugs was significantly stronger as compared to the effects obtained after individual administration of VEN or NIC. In the group exposed to tobacco smoke, joint administration of VEN–NIC induced a significant reduction of immobility as compared to the control and NIC groups. In the Morris Water Maze Test single and chronic administration of VEN, lower values of escape latencies and lower numbers of crossed quadrants were noted in both exposed and non–exposed rats, which indicates improved performance. After administering NIC we could observe improvement of spatial memory in both the exposed and non–exposed group. A similar effect of improvement of spatial memory was observed after joint administration of VEN and NIC. The study results support the involvement of nicotinic systems in memory processes in rats. Memory improvement and antidepressant effects following joint administration of VEN and NIC may depend on nicotinic interactions with monoaminergic systems and VEN may represent a new therapeutic approach to smoking cessation.

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