The effect of intraventricular gamma aminobutyric acid (GABA) on hypothalamic catecholamines and LHRH and on pituitary hormone release

Abstract

The present experiments were designed to evaluate the role of catecholamines in mediating the actions of GABA on pituitary hormone release following its intraventricular injection. GABA was administered intraventricularly, at doses of 0.1 and 4 μMol, to chronically ovariectomized rats. Five and 15 min after intraventricular injection, the animals were sacrificed by decapitation. Blood was collected for LH and PRL determination by RIA, and brains were frozen for subsequent determination of LHRH by RIA, and dopamine (DA) and norepinephrine (NE) by radioenzymatic assay. Brain areas analyzed included the median eminence (ME), medial basal hypothalamus (MBH) and suprachiasmatic-medial preoptic area (Sch-PO). Controls received an equal volume (2 μl) of saline. As previously observed, GABA had opposite effects on prolactin (PRL) release depending on the dose employed. A decline in serum PRL was induced by a low (0.1 μMol) dose, whereas a larger (4 μMol) dose induced an increase in PRL levels. LH levels were increased only with the 4 μMol dose. The elevated LH values were paralleled by an increase in LHRH levels in the Sch-PO region 15 min after GABA. Marked changes in catecholamines, particularly in DA, were seen after GABA injection. Significant increments in DA levels in the ME were seen 5 and 15 min after the 0.1 μMol dose of GABA. Similarly, this low dose of GABA induced a marked increase in DA levels in the anterior-pituitary (AP) gland at 15 min. No changes in DA were seen in either MBH or Sch-PO areas. The 4 μMol dose of GABA induced only a small increase in AP levels of DA, without altering the amine levels in any of the brain areas examined. NE levels in the ME were elevated 5 min after the administration of either dose of GABA. No changes in NE were seen in either the MBH or Sch-PO areas. These results indicate that intraventricular GABA injection not only alters pituitary hormone release but also release of DA and NE from terminals in the ME. The released catecholamines may be important in mediating the effects of GABA on releasing factor discharge. In addition, the DA released may have acted directly on the AP to inhibit release of PRL.