Neuronal Responses to Systemic Nicotine in the Solitary Tract Nucleus: Origin and Possible Relation with Nutritional Effects of Nicotine

Nicotinic receptor‐mediated effects on appetite and food intake

“…Nicotine-like many other anorexigenic substances, including leptin, CCK, and insulin-generally exerts opposite effects on the regulation of sympathetic outflow and appetite (Haynes et al, 1997;Yettefti et al, 1997;Niijima, 1998;Krisufek et al, 1999;Sha and Szurszewski, 1999;Bray, 2000). Thus, the net effects of nicotine include elevated blood pressure, heart rate, and gastric motility while eliciting a sustained decrease in food intake.…”

“…Systemic administration of nicotine stimulates visceral afferents and activates brain stem autonomic control centers, such as the solitary tract, ventrolateral medullary, and parabrachial nuclei (noted in Fig. 1 as NTS, VLM, and PBr, respectively; Yettefti et al, 1997;Bray, 2000;Cooper, 2001;Tribollet et al, 2001). Nicotineevoked responses are elicited in less than 25% of the NTS neurons when tested by direct ionotophoretic application, implicating both central and peripheral neuronal circuits in nicotine's effects on feeding (Yettefti et al, 1997).…”

“…1 as NTS, VLM, and PBr, respectively; Yettefti et al, 1997;Bray, 2000;Cooper, 2001;Tribollet et al, 2001). Nicotineevoked responses are elicited in less than 25% of the NTS neurons when tested by direct ionotophoretic application, implicating both central and peripheral neuronal circuits in nicotine's effects on feeding (Yettefti et al, 1997). Other studies underscore the contribution of nAChRs on cranial nerve and spinal cord visceral motor neurons in the regulation of sympathetic and parasympathetic outflow (e.g., McGehee et al, 1995;Tribollet et al, 2001).…”

"Efeito modulatório da nicotina sobre a neurotransmissão em núcleos encefálicos responsáveis pelo controle cardiovascular em ratos geneticamente hipertensos e normotensos"

“…Este fato é bastante explorado especialmente no estudo da dependência a drogas de abuso, como é o caso da nicotina (RYAN & LOIACONO, 2001;WOOLTORTON et al, 2003), e de doenças neurodegenerativas como a Doença de Parkinson (KELTON et al, 2000;QUIK, 2004). et al, 1977;MCNABB, 1984 Ainda considerando o peso dos animais, diversos trabalhos relatam perda de peso quando do tratamento crônico com nicotina (YETTEFTI et al, 1997;LI et al, 2000;CABANAC & FRANKHAM, 2002;FRANKHAM & CABANAC, 2003), correlacionada à estimulação da produção de NPY, orexinas e leptina (LI & KANE, 2003) ou mesmo excluindo-se a participação da leptina (SANIGORSKI et al, 2002). A utilização de ratos espontaneamente hipertensos (SHR) é bastante popular já que este é um dos modelos animais mais adequados para o estudo da hipertensão essencial (PINTO et al, 1998;AMENTA et al, 2003).…”