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.
journal_name
Life Scijournal_title
Life sciencesauthors
Barrios V,González-Parra S,Arilla Edoi
10.1016/0024-3205(92)90116-7subject
Has Abstractpub_date
1992-01-01 00:00:00pages
1991-8issue
25eissn
0024-3205issn
1879-0631pii
0024-3205(92)90116-7journal_volume
51pub_type
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