Isradipine inhibits nicotine intravenous self-administration in drug-naive mice

Martellotta, M.C.; Kuzmin, Alexander; Zvartau, Edwin; Cossu, G; Gl, Gessa; Fratta, Walter

doi:10.1016/0091-3057(95)00096-f

Cited by 49 publications

(30 citation statements)

References 13 publications

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“…Fourth, during the forcedintake studies (both bottles contained a nicotine solution) rats consumed between 13 and 19 mg/kg/day of nicotine without reducing their total fluid intake significantly (voluntary nicotine intake was only up to 2.2 mg/kg/day in the highest-consuming rat) indicating that the taste of nico-tine [26] could not have been overwhelmingly aversive. Fifth, operant self-administration of nicotine resulted in intakes of about 0.18-1.38 mg/kg/day [4,5,[19][20][21]27] which is very close to our intakes of 0.41-2.2 mg/kg/day. Sixth, using a 2-lever operant procedure, it could be shown that oral self-administration of nicotine can be used to assess nicotine preference [20].…”

Section: Discussionsupporting

confidence: 50%

Determinants of the Voluntary Consumption of Nicotine by Rats

Maehler

Dadmarz²,

Vogel³

2000

Neuropsychobiology

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The 2-bottle free-choice method was used to study the voluntary consumption of nicotine by rats. Rats consumed nicotine voluntarily at different, albeit quite consistent, amounts. Voluntary intakes were higher in younger than older rats, but were not affected by gender. A previously forced nicotine intake had no effect on a subsequent voluntary intake of nicotine in older but increased it in younger rats. Forced exposure to nicotine of pregnant and lactating rats did not increase the voluntary intake by their offsprings. Established free-choice drinking patterns of nicotine were not affected by a temporary forced intake of this substance. The 2-bottle choice proved to be a reliable method to study the voluntary intake of nicotine, and results suggest that nicotine is not ‘addictive’ per se, but that its use is apparently determined by the response of an individual rat to this substance.

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Section: Discussionsupporting

confidence: 50%

Determinants of the Voluntary Consumption of Nicotine by Rats

Maehler

Dadmarz²,

Vogel³

2000

Neuropsychobiology

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“…For example, the stimulation of DA release in the nucleus accumbens after several nicotine injections remains controversial Balfour et al, 1998;Di Chiara, 2000), and repeated nicotine treatments in rats induce a behavioral sensitisation, which vanishes quicker than for other drugs of abuse (Ksir et al, 1985;Villégier et al, 2003). Similarly, although self-administration of nicotine is observed in rodents (Corrigall and Coen, 1989;Donny et al, 1995;Martellotta et al, 1995;Shoaib et al, 1997;Caggiula et al, 2001) and monkeys (Goldberg et al, 1981;Wakasa et al, 1995), its development seems slower and weaker than for other drugs of abuse (Manzardo et al, 2002), and often needs facilitation by the use of food restriction (Corrigall et al, 2002;Rauhut et al, 2002) or cocaine pre-treatment (Picciotto et al, 1998). These differences suggest either that nicotine possesses both aversive and rewarding properties (Risinger and Brown, 1996;Shoaib et al, 2002), or that the addictive effects of tobacco are not only due to nicotine.…”

Section: Introductionmentioning

confidence: 99%

Monoamine Oxidase Inhibitors Allow Locomotor and Rewarding Responses to Nicotine

Villegier

Salomon

Granon

et al. 2005

Neuropsychopharmacol

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Although nicotine is generally considered to be the main compound responsible for the addictive properties of tobacco, experimental data indicate that nicotine does not exhibit all the characteristics of other abused substances, such as psychostimulants and opiates. For example, nicotine is only a weak locomotor enhancer in rats and generally fails to induce a locomotor response in mice. This observation contradicts the general consensus that all drugs of abuse release dopamine in the nucleus accumbens, a subcortical structure, and thus increase locomotor activity in rodents. Because tobacco smoke contains monoamine oxidase inhibitors (MAOIs) and decreases MAO activity in smokers, we have combined MAOIs with nicotine to determine whether it is possible to obtain a locomotor response to nicotine in C57Bl6 mice. Among 15 individual or combined MAOIs, including harmane, norharmane, moclobemide, selegiline, pargyline, clorgyline, tranylcypromine and phenelzine, only irreversible inhibitors of both MAO-A and -B (tranylcypromine, phenelzine, and clorgyline + selegiline) allowed a locomotor response to nicotine. The locomotor stimulant interaction of tranylcypromine and nicotine was absent in b2-nicotinic acetylcholine receptor subunit knockout mice. Finally, it was found that, whereas naïve rats did not readily selfadminister nicotine (10 mg/kg/injection), a robust self-administration of nicotine occurred when animals were pretreated with tranylcypromine (3 mg/kg). Our data suggest that MAOIs contained in tobacco and tobacco smoke act in synergy with nicotine to enhance its rewarding effects.

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“…The dose-response curve of contingent mice was similar to findings with cocaine, morphine, or nicotine (Kuzmin et al 1992;Martellotta et al 1995;Rasmussen and Swedberg 1998). Albeit the significant group by unit dose interaction demonstrates that increasing dose affected contingent and yoked control mice differently, a dosedependent increase in nose poking of yoked control mice suggests that nose poking of contingent mice was partly attributable to scopolamine-induced hyperactivity.…”

Section: Discussionmentioning

confidence: 53%

“…Scopolamine self-administration was demonstrated in a chronic rat model (Glick and Guido 1982), but there is no experimental evidence of possible acute effects of antimuscarinic self-administration. Because drug-naive mice self-administer cocaine, morphine, or nicotine (Kuzmin et al 1992;Martellotta et al 1995; Rasmussen and Swedberg 1998), we investigated if scopolamine could be self-administered in this model, suggesting similar acute and reinforcing properties.…”

mentioning

confidence: 99%