No abstract

A pharmacologic approach was used to examine the possible role of dopamine neurons in the regulation of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) secretion in the rat. Blockade of dopamine receptors by haloperidol or pimozide treatment evoked dose- and time-related increases in plasma levels of beta-END-LI. Physical immobilization increased circulating beta-END-LI six-fold and pretreatment with dopamine receptor agonists (bromocriptine or pergolide) significantly attenuated this rise without affecting plasma beta-END-LI levels in non-stressed animals. Dopaminergic drugs and immobilization produced similar effects on circulating PRL as on beta-END-LI. However, the magnitude of change in levels of PRL was generally greater than the change in beta-END-LI. The present findings suggest that dopaminergic neurons inhibit the release of pituitary beta-END-LI as well as PRL in the rat.