Prolactin stimulation of protein kinase C activity in the rat hypothalamus.
Stimulation of cultured hypothalamic slices with PRL causes a rapid translocation of a Ca2+/phospholipid dependent protein kinase from the cytosol to the membrane fraction. The translocation of PKC from the cytosol to the membrane occurred at physiological concentrations of PRL with a maximal response occurring at 10(-10) M. At concentrations above this, there was less PKC activity translocated from the cytosol to the membrane. When injected into the medial preoptic area of the hypothalamus, PRL resulted in a similar translocation of PKC activity. These data clearly indicate that PRL can activate PKC in the rat hypothalamus, and suggest that PKC may be one of the transmembrane signaling mechanisms involved in the regulation of brain function by prolactin.
DeVito
W J
WJ
Division of Endocrinology, University of Massachusetts Medical School, Worcester 01655.
Stone
S
S
Avakian
C
C
D000818:Animals; D001692:Biological Transport; D003600:Cytosol / Q000187:drug effects / Q000201:enzymology; D004305:Dose-Response Relationship, Drug; D005260:Female; D007031:Hypothalamus / Q000187:drug effects / Q000201:enzymology*; D011388:Prolactin / Q000008:administration & dosage / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D011388:Prolactin; D011493:Protein Kinase C