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Protein kinase C activators stimulate beta-endorphin secretion from hypothalamic cells.
L P Kapcala1, C F Weng, H H Juang
1Department of Medicine, University of Maryland, School of Medicine and Hospital, Baltimore 21201.
Brain Research Bulletin
|November 1, 1992
Summary
Protein kinase C (PKC) activators, including phorbol ester (PMA) and diacylglycerol (OAG), stimulate beta-endorphin secretion from the hypothalamus. Arginine vasopressin (AVP) and angiotensin II (Ang II) also increase beta-endorphin release.
Area of Science:
- Neuroendocrinology
- Cellular Signaling
Background:
- Hypothalamic beta-endorphin plays diverse physiological roles in the brain.
- Arginine vasopressin (AVP) stimulates beta-endorphin secretion via the phosphoinositol (PI) second messenger system.
Purpose of the Study:
- To investigate if protein kinase C (PKC) activators stimulate hypothalamic beta-endorphin secretion.
- To examine the effects of PKC stimulators (PMA, OAG) and other signaling pathway activators (AVP, Ang II, FSK) on beta-endorphin release.
Main Methods:
- Used dissociated fetal rat hypothalamic cell cultures.
- Measured immunoreactive (IR-) beta-endorphin secretion using radioimmunoassay (RIA).
- Administered phorbol ester (PMA), OAG, AVP, Ang II, and forskolin (FSK).
Main Results:
- PMA, OAG, AVP, and Ang II significantly stimulated IR-beta-endorphin secretion.
- Combined PMA and FSK (activator of cyclic AMP/protein kinase A pathway) showed an additive stimulatory effect on IR-beta-endorphin secretion, exceeding individual effects.
Conclusions:
- PKC activation is involved in the regulation of hypothalamic beta-endorphin secretion.
- Both PI and cyclic AMP signaling pathways modulate beta-endorphin release, with potential additive interactions.