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Effects of acute nicotine and mecamylamine administration on somatostatin concentration and binding in the rat brain

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Authors
Barrios Sabador, Vicente; Rodríguez Sánchez, María Nelly; Colás Escudero, María BegoñaUniversity of Alcalá Author; Arilla Ferreiro, EduardoUniversity of Alcalá Author
Identifiers
Permanent link (URI): http://hdl.handle.net/10017/2468
DOI: 10.1016/0014-2999(90)90164-2
ISSN: 0014-2999
Publisher
Elsevier
Date
1990
Affiliation
Universidad de Alcalá. Departamento de Bioquímica y Biología Molecular
Bibliographic citation
European Journal of Pharmacology, 1990, v. 179, n. 3, p. 263-270
Keywords
Rat
Brain
Mecamylamine
Nicotine
Somatostatin receptors
Project
PB87-0753 (Comisión Interministerial de Ciencia y Tecnología-CICYT)
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/10.1016/0014-2999(90)90164-2
Rights
© Elsevier Science Publishers, 1990
Access rights
info:eu-repo/semantics/openAccess
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Abstract
Since nicotine and somatostin have regulatory effects on locomotor activity it was of interest to determine whether the receptors for somatostin are modulated by the cholinergic nicotine-like effects. An i.v. dose of 0.3 mg/kg nicotine induced an increase in the concentrations of somatostatin-like immunoreactivity at 4 min in the parietal cortex and at 15 min in the hippocampus. These changes were associated with a significant increase in the total number of specific somatostatin receptors in the parietal cortex at 15 min and in the hippocampus at 30 min following injection. To determine if the above mentioned changes are related to the nicotine activation of central nicotine-like acetylcholine receptors, a cholinergic nicotinic blocking agent, mecamylamine, was administered before the nicotine injection. Pretreatment with mecamylamine (5.0 mg/kg i.v.) prevented the nicotine-induced changes in somatostatin level and binding in both brain areas. Mecamylamine alone had no observable effect on the somatostatinergic system. These results suggest that the somatostatinergic system can be regulated by nicotine-like acetylcholine receptors and may be involved in some of the behavioral central effects of nicotine.
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