Activation of cyclic AMP second messenger system stimulates secretion of beta-endorphin from fetal hypothalamic cells.
Relatively little is known about physiological regulators of hypothalamic beta-endorphin (END) secretion and mechanisms by which they stimulate secretion. We sought to determine whether activation of the cyclic AMP (cAMP) second messenger pathway was involved in stimulating hypothalamic beta-END secretion from dissociated fetal hypothalamic cells in culture. Forskolin (FSK), a direct activator of adenylate cyclase which stimulates cAMP formation, stimulated immunoreactive (IR)-beta-END secretion. Because FSK can also stimulate independent of increased cAMP formation, we studied dibutyryl cAMP and 8-bromo-cAMP, analogues of cAMP, which also stimulated IR-beta-END secretion. From these studies we conclude: (1) activation of the cAMP second messenger system stimulates IR-beta-END secretion from hypothalamic cells and supports the rationale that endogenous regulators which stimulate this pathway could be involved in the physiological regulation of hypothalamic beta-END secretion; (2) coupling between the cAMP second messenger pathway and stimulation of hypothalamic beta-END secretion which is presumably present at maturity (adulthood) originates at early stages of development (fetal life).
Kapcala
L P
LP
Department of Medicine, University of Maryland School of Medicine and Hospital, Baltimore 21201.
Weng
C F
CF
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism*; D005333:Fetus / Q000502:physiology; D007031:Hypothalamus / Q000166:cytology / Q000196:embryology / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D015290:Second Messenger Systems / Q000502:physiology*; D001615:beta-Endorphin / Q000378:metabolism*
D001615:beta-Endorphin; D000242:Cyclic AMP