Effects of tobacco and cigarette smoke extracts on serotonergic raphe neurons in the rat

Touiki, Khalid; Rat, Pascal; Molimard, R; Chait, Abderrahman; Beaurepaire, Renaud de

doi:10.1097/wnr.0b013e32811d6d21

Cited by 32 publications

(25 citation statements)

References 14 publications

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“…Such an effect may help explain the discrepancy between nicotine and tobacco extract effects observed in vitro (see Ambrose et al 2007 ;Touiki et al 2007), but has yet to be investigated in respect of the other minor tobacco alkaloids.…”

Section: Discussionmentioning

confidence: 95%

“…Interestingly, a tobacco extract containing all minor alkaloids produces greater nAChR-mediated inhibition of serotonergic neurons than nicotine alone, with nornicotine, anabasine and nicotine individually producing similar levels of inhibition (Touiki et al 2007). Furthermore, anabasine, cotinine, and nornicotine also elicit a calcium-dependent increase in striatal dopamine release through activation of the nAChR, and similarly to nicotine, produce nAChR desensitization (Dwoskin et al 1995 ;O'Leary et al 2008).…”

Section: Introductionmentioning

confidence: 97%

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The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats

Clemens¹,

Caillé²,

Stinus³

et al. 2009

Int. J. Neuropsychopharm.

127

137

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Several minor tobacco alkaloids have been found to exhibit properties pharmacologically relevant to the addictive profile of tobacco; however, little is known of their effects on a behavioural model of drug addiction. In this study we compared the locomotor and reinforcing effects of intravenous nicotine (30 microg/kg per infusion) vs. a cocktail of nicotine plus five minor alkaloids found in tobacco smoke (anabasine, nornicotine, anatabine, cotinine and myosmine). Rats were initially tested for their locomotor response to nicotine or nicotine plus the minor alkaloids with six intravenous injections over 1 h. We then assessed the spontaneous acquisition of intravenous self-administration with nicotine or nicotine plus the minor alkaloids, under a fixed-ratio 1 schedule followed by responding on a fixed-ratio 5 schedule, progressive-ratio schedule and a single within-session ascending dose-response test. The activity test was repeated following the progressive-ratio phase to assess locomotor sensitization. A second group of rats were then tested on the locomotor procedure to better clarify the role of each individual minor alkaloid in nicotine-induced locomotor activity. Compared to nicotine alone, addition of the minor tobacco alkaloids increased locomotor activity and increased locomotor sensitization following self-administration. During fixed-ratio 5, progressive ratio and the dose-response test, rats receiving nicotine plus the minor alkaloids responded significantly more than those receiving nicotine alone. Testing of each minor alkaloid in the second experiment indicated that anatabine, cotinine and myosmine individually increased nicotine-induced locomotor activity. These results suggest that the minor tobacco alkaloids, particularly anatabine, cotinine and myosmine, may increase the motivation for nicotine and thus facilitate smoking behaviour.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats

Clemens¹,

Caillé²,

Stinus³

et al. 2009

Int. J. Neuropsychopharm.

127

137

View full text Add to dashboard Cite

show abstract

“…CRF, endogenous opioids, and orexins). For details on the relevance of these diverse actions of NIC in various brain functions and in the development and maintenance of NIC dependence, (see De Biasi and Salas, 2008;Di Matteo et al, 2007;Touiki et al, 2007Touiki et al, , 2008Seth et al, 2002;Galindo-Charles et al, 2008;Rossi et al, 2005a,b;Grilli et al, 2005;Markou, 2007Markou, , 2008Liechti and Markou, 2008;Kenny et al, 2009;Hahn and Stolerman, 2005;Erhardt et al, 2000;George et al, 2007;Xue and Domino, 2008;Chen et al, 2008b;Merritt et al, 2008;Pasumarthi and Fadel, 2008).…”

Section: Relevance Of Dopamine In Nicotine Addictionmentioning

confidence: 98%

Smoking, nicotine and neuropsychiatric disorders

Döme

Lazáry

Kalapos³

et al. 2010

Neuroscience & Biobehavioral Reviews

197

140

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“…Particulate matter, derived from an ethanol extract of tobacco, produces similar effects to nicotine on locomotor activity (Brennan et al, 2013). Smoke extract, which contains many combustion products not present in tobacco leaf (Bates et al, 1999;Seeman et al, 2002), has been shown to have in vitro effects on dopamine neurons that are distinct from those of tobacco extract (Marti et al, 2011) and on serotonin neurons that are distinct from those of nicotine (Touiki et al, 2007). However, to date, there have been no studies of the behaviorally reinforcing effects of tobacco smoke extracts.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Reinforcing Properties of Nicotine and Cigarette Smoke Extract in Rats

Costello

Reynaga

Mojica

et al. 2014

Neuropsychopharmacol

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Tobacco dependence is difficult to treat, with the vast majority of those who try to quit relapsing within the first year. Improvements in smoking cessation therapies may be achieved by improving current preclinical research methods. However, most experimental tests in animals use nicotine alone, ignoring the 8000 other constituents found in tobacco smoke. To improve on this model, we have used selfadministration to test the reinforcing properties of aqueous cigarette smoke extract (CSE) in rats, made by bubbling cigarette smoke through a saline solution. CSE is more potent than nicotine alone in both the acquisition and maintenance of self-administration, but did not exhibit higher progressive ratio responding. Mecamylamine and varenicline had similar potencies to block nicotine and CSE selfadministration, indicating the involvement of nicotinic receptors in CSE reinforcement. Following extinction of responding, reinstatement was triggered by exposing animals to a pharmacological stressor, yohimbine (2.5 mg/kg, i.p.), alone and in combination with cues. Animals that self-administered CSE were significantly more sensitive to stress-induced reinstatement than those that self-administered nicotine. Ligand binding autoradiography studies showed nicotine and CSE to have similar affinities for different nicotinic receptor types. CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine did not. Although CSE inhibition of MAO-A activity in vitro was found to be partially irreversible, irreversible inhibition was not observed in vivo. These experiments show that CSE is an effective reinforcer acting via nicotinic receptors. Furthermore, it better models MAO inhibition and is more sensitive to stress-induced reinstatement than nicotine alone, which is a potent trigger for relapse in smokers.

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Effects of tobacco and cigarette smoke extracts on serotonergic raphe neurons in the rat

Cited by 32 publications

References 14 publications

The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats

The addition of five minor tobacco alkaloids increases nicotine-induced hyperactivity, sensitization and intravenous self-administration in rats

Smoking, nicotine and neuropsychiatric disorders

Comparison of the Reinforcing Properties of Nicotine and Cigarette Smoke Extract in Rats

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