Evidence for interaction between central beta-2 adrenoceptors and epinephrine patways in the opioid-induced prolactin rise in the rat

1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-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. Proctolol, 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