GABA and Muscimol Inhibit the Release of Prolactin from Dispersed Rat Anterior Pituitary Cells

Previous work from our laboratory showed that baclofen could lower serum prolactin (PRL) levels acting at the central nervous system. The present experiments were designed to evaluate whether the γ-aminobutyric acid B agonist was also effective in inhibiting hormone release at the pituitary level. In mono-layer cultures of adenohypophyseal dispersed cells, baclofen inhibited basal PRL secetion after 1 or 2 h of incubation. This inhibition was significantly abolished by three antagonists: phaclofen, 3-aminopropyl-phosphonic acid and 4-aminobutylphosphonic acid. Furthermore, baclofen inhibited the thyrotropin-releasing hormone-induced PRL release in a concentration-dependent manner. With regard to gonadotropin secretion, baclofen was unable to modify basal luteinizing hormone (LH) secretion, but significantly inhibited the LH-releasing hormone-induced LH release. These results show that baclofen, in addition to its central neuroendocrine effects, inhibits pituitary hormone secretion, under basal and/or stimulated conditions, by direct action at the pituitary level.

Section: Discussionsupporting

confidence: 57%

Activation of GABA B Receptors in the Anterior Pituitary Inhibits Prolactin and Luteinizing Hormone Secretion

Lux‐Lantos

Rey²,

Libertun³

1992

“…GABA has been found to affect the release of prolactin [6,9,10,15,19,24,25,29], LH [ 19,20] and growth hormone [31]. In the case of prolactin the effect of GABA appears to be a direct action at the level of the anterior pituitary [6,9,10, 29] via specific GABA receptors [9].…”

Section: Discussionmentioning

confidence: 99%

“…In the case of prolactin the effect of GABA appears to be a direct action at the level of the anterior pituitary [6,9,10, 29] via specific GABA receptors [9]. These results have suggested that GABA is released from the hypothalamus in to the portal system.…”

Section: Discussionmentioning

confidence: 99%

GABA Neuron Systems in Hypothalamus and the Pituitary Gland

Vincent¹,

Hökfelt²,

Wu³

1982

315

The distribution of γ-aminobutyric acid (GABA) nerve fibers and cell bodies in the rat hypothalamus and pituitary gland was immunohistochemically examined using antibodies against the GABA-synthesizing enzyme glutamate decarboxylase (GAD). A dense network of GAD-positive nerve fibers was observed to be essentially evenly distributed throughout the hypothalamus. A plexus of GABA terminals was also demonstrated both in the median eminence and within the posterior and intermediate lobes of the pituitary. Three distinct clusters of magnocellular GABA neurons were discovered in the posterior hypothalamus. In addition, GAD immunoreactive cell bodies were observed in many other hypothalamic nuclei, such as the arcuate nucleus and in the perifornical region. These results provide a morphological basis by which GABA of hypothalamic origin may regulate the neuroendocrine system.

“…GABA, like DA, was found to inhibit prolactin secretion at the adenohypophysial level [15,28,37,41]. This effect is probably mediated by high affinity receptors [14] which seem to act independently from DA receptors [11].…”

Section: Discussionmentioning

confidence: 95%

Benzodiazepine Antagonist Ro 15-1788 Counteracts the Prolactin-Lowering Effects of Other Benzodiazepines in Rats

Lotz¹

1982

A number of centrally active benzodiazepines lowered baseline serum prolactin concentrations after oral administration to male rats. The increase of circulating prolactin levels elicited by oral administration of various neuroleptic agents was also reduced by prior or simultaneous oral administration of several benzodiazepines in a dose-dependent manner. Since both effects were prevented by simultaneous administration of the benzodiazepine antagonist Ro 15-1788 they are probably mediated by central benzodiazepine receptors which interfere with aminergic mechanisms governing serum prolactin.