Induction of glucocorticoid receptor expression in hypothalamic magnocellular vasopressin neurons during chronic hypoosmolality.
The site of action for the modulation of hypothalamo-neurohypophyseal function by adrenal steroids is not known. Glucocorticoid receptors (GR) are an obvious potential site of action, but there have been conflicting reports of GR localization in magnocellular neurons. We confirm studies finding undetectable levels of GR in vasopressin or oxytocin neurons, but now report that chronic hypoosmolality induces the expression of GR in magnocellular vasopressin neurons, but not oxytocin neurons. These data support the hypothesis that the vasopressin gene can be directly inhibited by glucocorticoids, and that the induction of GR expression in magnocellular neurons may be part of a redundant set of mechanisms to suppress the expression of AVP during periods of prolonged hypoosmolality. This mechanism represents a novel form of steroid feedback control in brain.
Department of Neuroscience, University of Pittsburgh, PA 15260.
K A
KA
Berghorn
L T
LT
Knapp
G E
GE
Hoffman
T G
TG
Sherman
D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000378:metabolism*; D009994:Osmolar Concentration; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000096:biosynthesis*; D012964:Sodium / Q000097:blood
D011965:Receptors, Glucocorticoid; D001127:Arginine Vasopressin; D012964:Sodium