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Abstract: Little is known about biological factors involved in post-stroke smoking cessation. A recent retrospective study has indicated a possible association between unilateral insular lesions of various origin and a rapid disruption of nicotine addiction. Given the above, the aim of the present prospective study was to assess a relationship between post-stroke smoking cessation and lesion localization. Eighty-seven patients with first-ever, unilateral, ischemic stroke who had been active smokers at stroke onset were examined during hospitalization and at 3-month follow-up. No association was found between any specific lesion localization (the insula, operculum, striatum, thalamus, internal capsule, brainstem) and smoking status at the 3-month follow-up visit. Patients with lacunar circulation strokes (LACS) were more likely to be non-smokers at the follow-up examination. No sudden disruption of nicotine addition was observed in patients with insular or other stroke locations. Concluding, post-stroke smoking cessation may not be associated with insular lesions. [Copyright &y& Elsevier]

Abstract: Low doses of ethanol may antagonize the pharmacological effects of nicotine. Recently, it has been shown that the effects of ethanol on nicotine discrimination are not correlated with blood ethanol levels. The aim of the present study was to evaluate whether ethanol (0.5–2g/kg, i.p.) could block nicotine-induced seizures in C57BL/6J mice and to correlate ethanol''s actions with blood ethanol concentrations. For comparison, the effects of a γ-aminobutyric acid A (GABAA)/benzodiazepine receptor positive modulator, midazolam (0.25–40mg/kg, i.p.), and a γ-aminobutyric acid B receptor agonist, baclofen (2.5–20mg/kg, i.p.), were assessed in the same procedure. Nicotine (3–9mg/kg, s.c.) induced clonic–tonic seizures in a dose-dependent manner. Ethanol, administered 5 or 50min before nicotine, dose dependently antagonized seizures elicited by 6mg/kg nicotine. The anticonvulsant effects of ethanol correlated with blood ethanol levels and were comparable to those exerted by midazolam. Baclofen antagonized only the tonic component of nicotine-induced convulsions. The anticonvulsant doses of ethanol (0.5–2g/kg), midazolam (0.5–1mg/kg), and baclofen (5–10mg/kg) did not affect spontaneous locomotor activity in a control experiment. The present results indicate that (i) ethanol may block nicotine-induced seizures in mice at doses that do not alter locomotor activity and (ii) the antiseizure effects of ethanol depend on blood ethanol levels and are comparable to those exerted by the GABAA positive modulator midazolam. [Copyright &y& Elsevier]