RESUMEN
Experimental methodssintraperitoneal injection of diazepam,r-aminobutyric acid (GABA) receptor antagonist (picrotoxin) and GABA synthesis inhibitor (iso-niazid) ;the pain threshold and serotonin ( 5 -HT) content in the brain are measured with spectrofluorometry.The effect of diazepam on ACTH analgesia (AA) is abstracted and the possible mechanisms of diazepam effect are studied.Results: diazepam increases the effect of AA.picroloxin and isoniazid reduce it and antagonize the analgesia effect of ACTH; diazepam increases the content of 5-HT in hipocampus,hypothalamus and midbrain;diazepam + ACTH increases,more than AC-TH or diazepam singly,the level of 5-HT in the 3 brain regions; picrotoxin and isoniazid reverse the effect of diazepam and ACTH on the content of 5-HT in the 3 brainsites; potentiation of diazepam on AA is antagonized by naloxone and atropine.
RESUMEN
The present experiments were carried out to further elucidate the mechanism by which dopamine mediates the actions of Y-aminobutyric acid on prolactin release from anterior pituitary following its intraventricular injection in overiectomized conscious rats, YAminobutyric acid significantly suppressed the prolactin levels at 0.1 μmol concentration while at 4 μmol dose, the level was elevated. The activity of tyrosine hydroxylase was increased significantly in the anterior pituitary at the lower dose while the higher concentration of Yaminobutyric acid did not bring about any change in the activity both in the hypothalamus and the anterior pituitary. The results presented suggest that intracellular dopamine in the anterior pituitary may directly inhibit prolactin release; the plasma prolactin level is elevated by Yaminobutyric acid, by way of either inhibiting dopaminergic tone or possible stimulation of a physiological prolactin releasin g hormone.