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Acute nicotine administration increases somatostatin content and binding in the rat hypothalamus

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Authors
Barrios Sabador, Vicente; Gonzalez-Parra, S.; Arilla Ferreiro, EduardoUniversity of Alcalá Author
Identifiers
Permanent link (URI): http://hdl.handle.net/10017/2439
DOI: 10.1016/0024-3205(92)90116-7
ISSN: 0024-3205
Publisher
Pergamon Press
Date
1992
Affiliation
Universidad de Alcalá. Departamento de Bioquímica y Biología Molecular
Bibliographic citation
Life Sciences, 1992, vol. 51, n. 25, p. 1991-1998
Keywords
Nicotine
Somatostatin
Hypothalamus
Project
PM91-0027 (Ministerio de Educación y Ciencia)
88/0903 (Fondo de Investigaciones Sanitarias -FIS)
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/publishedVersion
Publisher's version
http://dx.doi.org/10.1016/0024-3205(92)90116-7
Rights
(c) Pergamon Press, 1992
Access rights
info:eu-repo/semantics/openAccess
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Abstract
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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