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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nicotinic acetylcholine receptor (nAChR) subtypes alpha4beta2 and alpha7 comprise the majority of brain nicotine-binding sites. Classical genetic strategies using inbred mice and their hybrids suggest that nicotine's effects on locomotor activity and body temperature are influenced by alpha4beta2 but not alpha7 receptors. To evaluate directly the role of these nicotinic subtypes on responses to nicotine, beta2 and alpha7 null mutant (-/-) mice, as well as wild-type (+/+) and heterozygous (+/-) mice, were tested for baseline body temperature and locomotion and nicotine (0-1.5 mg/kg)-induced changes in these responses. Basal responses for these measures were similar for all beta2 genotypes, but baseline Y-maze activity was higher in alpha7-/- mice compared with alpha7+/+ mice. Following nicotine injection, dose-dependent decreases in body temperature and locomotor activity were observed for all three genotypes of both beta2 and alpha7 mice. Although responses in alpha7 mice did not differ among genotypes, beta2 gene deletion was found to have a gene-dependent effect on nicotine's effects. beta2-/- mice were less sensitive to nicotine-induced locomotor depression and hypothermia at low nicotine doses (.25-.5 mg/kg) but were no different from beta2+/+ mice at the highest doses tested (1.0-1.5 mg/kg). Residual responses at high nicotine doses in beta2-/- mice as well as responses in all alpha7 and beta2 mouse genotypes were mediated by nicotinic receptors, since mecamylamine (1.0 mg/kg) blocked all responses following 1.0 mg/kg nicotine. This finding suggests receptors that include the beta2 nAChR subunit partially mediate nicotine's effects on locomotor activity and body temperature.
Nicotine Tob Res 2004 Feb
PMID:Null mutant analysis of responses to nicotine: deletion of beta2 nicotinic acetylcholine receptor subunit but not alpha7 subunit reduces sensitivity to nicotine-induced locomotor depression and hypothermia. 1498 98

Menthol is a commonly used additive in tobacco products. Smoking cessation may be more difficult for smokers of mentholated cigarettes, particularly adolescent smokers. Evidence indicates that menthol can influence neurotransmitter receptors and nicotine metabolism. We investigated the effects of chronic menthol using body temperature as a bioassay for the effects of acute nicotine in vivo. Male rats (34-36 days, adolescent; 53-58 days, young adult; 9-10 months, full adult) were injected with menthol (100 mg/kg) or vehicle once daily for 4 days. On day 5, animals were injected with nicotine (0.5 mg/kg) and body temperature was measured for the next 70 min. We found no effect of chronic menthol treatment or of age on baseline temperature. Nicotine quickly produced vasodilatory hypothermia in all animals. Chronic menthol treatment had significant effects only in adolescent rats, diminishing nicotine-induced hypothermia. Nicotine treatment was repeated on day 6 to test for tolerance. Equivalent tolerance was found in all ages, and the attenuating effect of menthol was still present and was still limited to adolescent rats. In adolescents, acute menthol injection (400 mg/kg) 30 min prior to nicotine also attenuated nicotine-induced hypothermia but with a smaller effect size. Also in adolescents, we found no effect of chronic or acute menthol on hypothermia induced by hydralazine, a peripherally acting vasodilator. These data demonstrate that menthol diminishes the influence of nicotine on body temperature in adolescents, suggesting a greater susceptibility of youthful physiology to menthol.
Nicotine Tob Res 2008 Dec
PMID:Chronic menthol attenuates the effect of nicotine on body temperature in adolescent rats. 1902 26