γ-Aminobutyric Acid Inhibitsβ-Endorphin Secretion from the Anterior Pituitary but not the Neurointermediate Lobe in the Rat

Publisher Website
Google Scholar
Abstract
We have evaluated the role of .gamma.-aminobutyric acid (GABA) in the neuroendocrine control of .beta.-endorphin (.beta.-EP) secretion in the rat. Plasma .beta.-EP and .beta.-lipotropin (.beta.-LPH) levels and .beta.-EP-like immunoreactivity (.beta.-EPLI) in the anterior pituitary (AP) and neurointermediate lobe (NIL) were determined after administration of GABA antagonist or agonist drugs in male rats under resting conditions or after potent physical stresses. Bicuculline (0.1-0.8 mg/kg BW ip), a GABA receptor antagonist, induced a dose-related rise in plasma .beta.-EP and .beta.-LPH levels and a concomitant decrease in .beta.-EPLI concentrations in the AP but not in the NIL. Muscimol, a potent GABA-mimetic drug, did not alter baseline plasma .beta.-EP and .beta.-LPH levels, whether given systemically (1.0-2.0 mg/kg BW ip) or intracerebroventricularly (500 ng/kg BW), but prevented the effect of bicuculline on plasma and AP-.beta.-EP and .beta.-LPH concentrations. Administration of foot shock or restraint stress induced a clear-cut activation of the AP-related .beta.-EP secretion, an effect that was prevented by pretreatment with muscimol. Together, these data show that GABA-ergic mechanisms, probably operating at a central nervous system level, exert an inhibitory action on resting and stimulated .beta.-EP and .beta.-LPH secretion. Since no alterations of .beta.-EP concentrations in the NIL occurred after manipulations with GABA-ergic drugs or stress, and these were detected only in the AP, an interaction between GABA-ergic neurons and CRF neurons is the most likely explanation for the reported findings.