Abstract
Adult Wistar male rats underwent immobilization stress (IS) during forty minutes. PRL secretion presented a remarkable increase after 5 minutes, and it was higher than pre-stress values during the entire duration of the experiment. The blockade of beta-1 adrenoceptors by icv injections of practolol did not modify IS-induced PRL release. IPS 339, a selective antagonist of beta-2 adrenoceptors, also injected icv, reduced PRL secretion during stress in a dose dependent fashion. The blockade of PRL secretion due to IPS 339 was reverted by a previous icv administration of salbutamol, a classical beta-2 agonist. The data presented here suggest that central beta-2 adrenoceptors activation is an important step in the control of stress-induced PRL secretion.
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