Osmoresponsive units in sheep median preoptic nucleus

Abstract

Single-unit neural activity in the lamina terminalis, a region implicated in osmoregulation, was studied in alpha-chloralose-anesthetized sheep during mild hyperosmotic stimulation (intracarotid infusions of 1.65 M NaCl, 3 M sorbitol in 0.15 M NaCl, or 3 M urea in 0.15 M NaCl, at 1 ml/min). Twelve of 121 units (9.9%) were activated significantly (by 82 +/- 52%) by 2- to 3-min infusions of 1.65 M NaCl. Eleven of these and one untested unit were excited by hypertonic sorbitol (91 +/- 40% increase). Of five units further tested with urea, two were excited (by 19 and 58%). Isotonic or hypotonic NaCl infusions were without effect (eight osmoresponsive units tested). All responsive units were in the median preoptic nucleus (MnPO; nucleus medianus). MnPO units were compared with neurohypophysial fibers (multiunit recordings). Osmotic response profiles were similar; both MnPO units and neurohypophysial fibers responded equally to hypertonic NaCl and sorbitol but less to equiosmolal urea. Both MnPO units and neurohypophysial fibers responded slowly, taking 50 and 30 s of NaCl infusion, respectively, to show significant increases and approximately 2 min to reach peak activity. Their hemodynamic responses differed, however; neurohypophysial fibers were strongly excited by nitroprusside-induced hypotension (three of three animals) but MnPO osmoresponsive units were not (zero of five units). Osmoresponsive MnPO units may contribute osmotic, but not hemodynamic, inputs to control vasopressin secretion and/or osmoregulatory responses.

Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus

“…These observations are consistent with the ability of these stimuli to increase neuronal discharge of MnPO neurons in vivo (McAllen et al, 1990;Tanaka et al, 1995;Aradachi et al, 1996;Stocker and Toney, 2005). In addition, changes in circulating blood volume have been reported to increase Fos immunoreactivity in MnPO neurons (Potts et al, 2000).…”

“…In some cases, Fos immunoreactivity was reported in MnPO neurons that project to the hypothalamic paraventricular nucleus (PVH) and/or supraoptic nucleus (Oldfield et al, 1994;Larsen and Mikkelsen, 1995). Consistent with the notion that osmolality and ANG II increase the excitability of MnPO neurons, electrophysiological studies in vivo have demonstrated that hyperosmolality and circulating ANG II significantly increased the neuronal firing rates of MnPO neurons (McAllen et al, 1990;Tanaka et al, 1993;Tanaka et al, 1995;Aradachi et al, 1996;Stocker and Toney, 2005).…”

“…In this regard, our laboratory (Stocker and Toney, 2005) and others (Knuepfer et al, 1985;McAllen et al, 1990;Tanaka et al, 1993;Tanaka et al, 1995;Aradachi et al, 1996) have shown that MnPO neurons are responsive to changes in plasma osmolality, circulating ANG II, and/or changes in ABP. Since the central nervous system integrates these stimuli along with the prevailing level of blood volume to result in appropriate behavioral, neuroendocrine, and autonomic responses to body fluid homeostatic challenges, we examined whether the ongoing activity of MnPO neurons is altered by activation of vagal afferent fibers and whether vagal afferent input specifically targeted MnPO-PVH neurons that were responsive to forebrain ANG II and osmotic stimulation.…”

Transient Receptor Potential Vanilloid 1 Is Required for Intrinsic Osmoreception in Organum Vasculosum Lamina Terminalis Neurons and for Normal Thirst Responses to Systemic Hyperosmolality

“…A second possibility is that CNS areas other than the OVLT can contribute to the osmotic modulation of thirst. Indeed, osmosensitive and Na ϩ -sensitive neurons have been found in the subfornical organ (Anderson et al, 2001) and in the median preoptic nucleus (McAllen et al, 1990;Travis and Johnson, 1993;Grob et al, 2004), areas known to be part of the integrated neural circuit that underlies osmoregulation (Johnson and Gross, 1993). Finally, it is possible that our protocol did not lead to a pure osmotic stimulus and that additional (i.e., non-osmotic) factors contributed to the thirst response.…”

Endogenous angiotensin II facilitates GABAergic neurotransmission afferent to the Na+-responsive neurons of the rat median preoptic nucleus

“…Changes in plasma osmolality have been shown to alter the spiking activity of MnPO neurons (1,29,37,38), and our laboratory discovered that these changes in electrical activity of MnPO neurons were driven by changes in the cerebrospinal fluid (CSF) Na ϩ level, rather than CSF osmolality (14). Behavioral studies showed that ANG II infused into the OVLT or adjacent MnPO caused an increase in Na ϩ intake (8,10,11).…”