Acute nicotine administration increases somatostatin content and binding in the rat hypothalamus
Identificadores
Enlace permanente (URI): http://hdl.handle.net/10017/2439DOI: 10.1016/0024-3205(92)90116-7
ISSN: 0024-3205
Editor
Pergamon Press
Fecha de publicación
1992Cita bibliográfica
Life Sciences, 1992, vol. 51, n. 25, p. 1991-1998
Palabras clave
Nicotine
Somatostatin
Hypothalamus
Proyectos
PM91-0027 (Ministerio de Educación y Ciencia)
88/0903 (Fondo de Investigaciones Sanitarias -FIS)
Tipo de documento
info:eu-repo/semantics/article
Versión
info:eu-repo/semantics/publishedVersion
Versión del editor
http://dx.doi.org/10.1016/0024-3205(92)90116-7Derechos
(c) Pergamon Press, 1992
Derechos de acceso
info:eu-repo/semantics/openAccess
Resumen
Within 4 minutes a single, intravenous injection of nicotine (0.3 mg/Kg) induced increases in somatostatin-like immunoreactivity concentrations in the rat hypothalamus but not in the striatum. These changes were associated with a significant increase in the specific binding of somatostatin to putative receptor sites in hypothalamic membranes, while no significant changes were found in striatum. The enhancement of somatostatin binding resulted from a rapid increase in the number of available receptors rather than a change in receptor affinity. This effect appears to be mediated by nicotinic cholinergic receptors, because pretreatment with a centrally active nicotinic receptor antagonist, mecamylamine (5.0 mg/Kg i.v.), prevented the nicotine-induced changes in somatostatin content and binding in the hypothalamus. Mecamylamine alone had no observable effect on the hypothalamic somatostatinergic system. These results suggest that the rat hypothalamic somatostatinergic system can be regulated by nicotine-like acetylcholine receptors.
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