γ‐Amino Butyric Acid Control of Arginine Vasopressin Release from the Ewe Hypothalamus In Vitro: Sensitivity to Oestradiol

Abstract

The present study aims to ascertain the influence of gamma-amino butyric acid (GABA)(A or B) receptors on arginine vasopressin (AVP) release in vitro and determine whether E(2) modulates GABA-AVP interaction. Within 10 min of ewe killing, saggital midline hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus along with the median eminence, 2-mm thick, two per ewe) were dissected, placed in oxygenated minimum essential media (MEM)-alpha at 4 degrees C and within 2 h were singly perifused at 37 degrees C with oxygenated MEM-alpha (pH 7.4; flow rate 0.15 ml/min), either with or without E(2) (24 pg/ml). After 4-h equilibration, 10-min fractions were collected for 4 h interposed with a 10-min exposure at 60 min to a specific GABA(A or B) receptor agonist or antagonist at various doses (0.1-10 mm). GABA(A) (muscimol; no E(2), n = 7 perifusion chambers, with E(2), n = 11) or GABA(B) (baclofen; no E(2), n = 8, with E(2), n = 15) agonists (10 mm) did not influence AVP concentrations. However, AVP release increased (p < 0.05) 20-30 min after exposure to 10 mm GABA(A or B) antagonists (bicuculline, no E(2), n = 7: from 4.6 +/- 0.7 to 33.0 +/- 0.4, with E(2), n = 17: from 11.9 +/- 1.4 to 32.8 +/- 6.0; CGP52432, with E(2), n = 14: from 14.0 +/- 2.6 to 28.8 +/- 3.9 pg/ml). At the end of the collection period, hypothalamic slices responded to KCl (100 mm) with AVP efflux (p < 0.05). GABA(B) but not GABA(A) antagonist-stimulated AVP release was enhanced in the presence of E(2). In summary, AVP release is under the inhibitory influence of GABA input with further potentiation by E(2) through GABA(B) receptors in vitro.

Noradrenergic Control of Arginine Vasopressin Release from the Ewe Hypothalamus In Vitro: Sensitivity to Oestradiol

“…However, the presence or absence of E 2 did not affect the initial responses to the α 1 ‐adrenoreceptor agonist or antagonist in the present study. Following earlier observations (Ghuman et al. 2007), it is hypothesized that noradrenergic systems interact with GABA systems to suppress AVP secretion in the presence of E 2 .…”

“…However, the presence or absence of E 2 did not affect the initial responses to the a 1 -adrenoreceptor agonist or antagonist in the present study. Following earlier observations (Ghuman et al 2007), it is hypothesized that noradrenergic systems interact with GABA systems to suppress AVP secretion in the presence of E 2 . In the rat, GABA A receptor activation inhibits parvocellular PVN neurones and such tonic inhibition is enhanced by activation of a 1 -adrenoreceptors on GABA neurones (Han et al 2002).…”

“…2002). In the ewe, E 2 potentiates inhibition of AVP through GABA B (but not GABA A ) receptors resulting overall in additional inhibition of AVP neurones in the presence of E 2 through the combined influence of both GABA A and GABA B receptors (Ghuman et al. 2007).…”

“…In the rat, GABA A receptor activation inhibits parvocellular PVN neurones and such tonic inhibition is enhanced by activation of a 1 -adrenoreceptors on GABA neurones (Han et al 2002). In the ewe, E 2 potentiates inhibition of AVP through GABA B (but not GABA A ) receptors resulting overall in additional inhibition of AVP neurones in the presence of E 2 through the combined influence of both GABA A and GABA B receptors (Ghuman et al 2007). Taken together, the evidence explains the a 1 -adrenoreceptor-mediated suppression of AVP in the presence of E 2 (Fig.…”

Involvement of hypothalamic paraventricular nucleus non‐N‐methyl‐d‐aspartate receptors in the pressor response to noradrenaline microinjected into the bed nucleus of the stria terminalis of unanesthetized rats

“…Therefore, BST‐GABAergic neurons could project to glutamatergic neurons in the periPVN region, and their inhibition because of activation of α 1‐ and α 2 ‐adrenoceptors in the BST could result in deinhibition of glutamatergic inputs to the PVN and activation of magnocellular neurons. This idea is reinforced by in‐vitro results showing that administration of a GABA receptor antagonist in hypothalamic slices (from the anterior preoptic area to the mediobasal hypothalamus along with the median eminence) increases vasopressin release (Ghuman et al. , 2007).…”