Presynaptic α-adrenoceptors in median preoptic nucleus modulate inhibitory neurotransmission from subfornical organ and organum vasculosum lamina terminalis

The median preoptic nucleus (MnPO) in the lamina terminalis receives a prominent catecholaminergic innervation from the dorsomedial and ventrolateral medulla. The present investigation used whole cell patch-clamp recordings in rat brain slice preparations to evaluate the hypothesis that presynaptic adrenoceptors could modulate GABAergic inputs to MnPO neurons. Bath applications of norepinephrine (NE; 20–50 μM) induced a prolonged and reversible suppression of inhibitory postsynaptic currents (IPSCs) and reduced paired-pulse depression evoked by stimulation in the subfornical organ and organum vasculosum lamina terminalis. These events were not correlated with any observed changes in membrane conductance arising from NE activity at postsynaptic α1- or α2-adrenoceptors. Consistent with a role for presynaptic α2-adrenoceptors, responses were selectively mimicked by an α2-adrenoceptor agonist (UK-14304) and blockable with an α2-adrenoceptor antagonist (idazoxan). Although the α1-adrenoceptor agonist cirazoline and the α1-adrenoceptor antagonist prazosin were without effect on these evoked IPSCs, NE was noted to increase (via α1-adrenoceptors) or decrease (via α2-adrenoceptors) the frequency of spontaneous and tetrodotoxin-resistant miniature IPSCs. Collectively, these observations imply that both presynaptic and postsynaptic α1- and α2-adrenoceptors in MnPO are capable of selective modulation of rapid GABAA receptor-mediated inhibitory synaptic transmission along the lamina terminalis and therefore likely to exert a prominent influence in regulating cell excitability within the MnPO.

Osmotic regulation of estrogen receptor-β expression in magnocellular vasopressin neurons requires lamina terminalis

Estrogen receptor-β (ER-β) expression in rat magnocellular vasopressin (VP) neurons of the supraoptic and paraventricular nuclei (SON and PVN, respectively) becomes undetectable after 72 h of 2% NaCl consumption. To test the hypothesis that osmosensitive mechanisms that originate in the region of the organum vasculosum lamina terminalis (OVLT) control ER-β expression in the SON and PVN, animals were water deprived after electrolytic lesions were performed on the area anterior to the ventral third ventricle (AV3V). Such lesions prevent osmotic stimulation of VP release. Four weeks after surgery, male rats [lesioned ( n = 16) or sham ( n = 14)] were water deprived for 48 h or allowed water ad libitum. Water deprivation eliminated ER-β-immunoreactivity (-ir) in SON and magnocellular PVN of sham-lesioned animals. Fos-ir was evident in these neurons, and plasma osmolality (Posm) and hematocrit (Ht) were significantly elevated compared with the sham-hydrated rats (Posm, 304 ± 1 vs. 318 ± 2 mosmol/kgH2O; P < 0.001; Ht, 49.6 ± 0.6 vs. 55.0 ± 0.9%; P < 0.001). ER-β expression was comparable in sham-hydrated, AV3V-hydrated, and 6 of 8 AV3V-dehydrated rats despite significant increases in Posm in both groups (AV3V hydrated, 312 ± 2; AV3V dehydrated, 380 ± 10 mosmol/kgH2O; P < 0.001). OVLT was not ablated in the AV3V-dehydrated rats in which ER-β was depleted. Fos-ir was low or undetectable in SON in the AV3V-hydrated animals despite elevated Posm values. In AV3V-dehydrated rats, Fos-ir was significantly less than in sham-dehydrated animals but was significantly increased compared with the sham-hydrated group. This could reflect activation by nonosmotic parameters that do not inhibit ER-β expression. These data support the hypothesis that inhibition of ER-β expression in the SON by osmotic stimulation is mediated by osmoreceptive neurons in the lamina terminalis.