Long-term haloperidol treatment elevates beta-endorphin levels in the intermediate pituitary but not in rat brain.
Long-term treatment of rats with haloperidol, a dopamine receptor antagonist, produced a dose-dependent increase in immunoreactive beta-endorphin (i beta-END) concentrations in the neurointermediate lobe of the pituitary (NIL). In contrast, chronic haloperidol treatment had no significant effect on i beta-END levels in the hypothalamus, the midbrain or in discrete, microdissected brain nuclei even when administered at a dose (5 mg/kg) ten-fold higher than that which elevated i beta-END levels in the NIL. Chronic treatment with bromocriptine, a dopamine receptor agonist, had the opposite effect on the NIL, lowering i beta-END levels to approximately one-third of control values, but it did not affect hypothalamic i beta-END concentrations. These data are consistent with prior evidence that the synthesis of beta-END by IL melanotrophs is reciprocally modulated by dopaminergic ligands. The results indicate, however, that beta-END-releasing neurons are not similarly regulated.
Millington
W R
WR
Maiewski
S
S
O'Donohue
T L
TL
Mueller
G P
GP
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism*; D004723:Endorphins / Q000378:metabolism*; D006220:Haloperidol / Q000494:pharmacology*; D007700:Kinetics; D008297:Male; D009928:Organ Specificity; D010902:Pituitary Gland / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D001615:beta-Endorphin
D004723:Endorphins; D001615:beta-Endorphin; D006220:Haloperidol