Evidence for interaction between central beta-2 adrenoceptors and epinephrine pathways in the opioid-induced prolactin rise in the rat
De Castro-e-Silva, E.; Antunes-Rodrigues, J.
Brazilian Journal of Medical and Biological Research 21(5): 1057-1063
1988
ISSN/ISBN: 0100-879X PMID: 3248234 Document Number: 308900
1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-induced prolactin (PRL) rise was investigated. 2. FK 33824, a synthetic opioid peptide injected into the third ventricle of Wistar male rats, generated a PRL rise that was significantly reduced by pretreatment with IPS 339, a potent and selective beta-2 antagonist. 3. Inhibition of central epinephrine synthesis with SKF 64 139, which selectively blocks phenylethanolamine-N-methyltransferase, partially decreased the PRL release induced by FK 33824. 4. Practolol, a selective beta-1 adrenoceptor blocker, did not modify the PRL secretion induced by FK 33824. 5. The results indicate that this FK 33824-induced PRL rise depends in part on the functional integrity of central beta-2 adrenoceptors and that epinephrine pathways in the brain may play an important role in the mechanisms by which opioid peptides increase PRL secretion.