Search

Located in the midline lamina terminalis of the anterior wall of the third ventricle, the median preoptic nucleus is a thin elongated nucleus stretching around the rostral border of the anterior commissure. Its neuronal elements, composed of various types of excitatory glutamatergic and inhibitory GABAergic neurons, receive afferent neural signals from (1) neighboring subfornical organ and organum vasculosum of the lamina terminalis related to plasma osmolality and hormone concentrations, e.g., angiotensin II; (2) from peripheral sensors such as arterial baroreceptors and cutaneous thermosensors. Different sets of these MnPO glutamatergic and GABAergic neurons relay output signals to hypothalamic, midbrain, and medullary regions that drive homeostatic effector responses. Included in the effector responses are (1) thirst, antidiuretic hormone secretion and renal sodium excretion that subserve osmoregulation and body fluid homeostasis; (2) vasoconstriction or dilatation of skin blood vessels, and shivering and brown adipose tissue thermogenesis for core temperature homeostasis; (3) inhibition of hypothalamic and midbrain nuclei that stimulate wakefulness and arousal, thereby promoting both REM and non-REM sleep; and (4) activation of sympathetic pathways that drive vasoconstriction and heart rate to maintain arterial pressure and the perfusion of vital organs. The small size of MnPO belies its massive homeostatic significance., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Mammals are characterized by a stable core body temperature. When maintenance of core temperature is challenged by ambient or internal heat loads, mammals increase blood flow to the skin, sweat and/or pant, or salivate. These thermoregulatory responses enable evaporative cooling at moist surfaces to dissipate body heat. If water losses incurred during evaporative cooling are not replaced, body fluid homeostasis is challenged. This article reviews the way mammals balance thermoregulation and osmoregulation.

Suppression of vasopressin secretion to very low levels is essential for the excretion of excess water. To investigate a role for the preoptic brain region in the suppression of vasopressin secretion and the excretion of a water load, lesions were made in the vicinity of the lamina terminalis in ewes (LTX-sheep) and responses to water-loading or reduction of cerebrospinal fluid NaCl by i.c.v. isotonic mannitol solution were investigated. In normal conscious sheep, intraruminal water-loading resulted in the urine flow rate increasing and urine osmolality decreasing within 1 h, such that renal free water clearance (CH 2O ) increased from -1.02 ± 0.16 ml/min (mean ± SEM) to a maximum of +4.99 ± 0.62 ml/min at 2.5 h after water-loading (P < 0.05, n = 6). Plasma vasopressin levels fell from 0.88 ± 0.17 pg/ml to undetectable levels (< 0.4 pg/ml, n = 4). In LTX-sheep (n = 6), CH 2O did not change significantly after water-loading (-1.78 ± 0.13 to -2.03 ± 0.49 ml/min at 2.5 h after water-loading). Plasma vasopressin levels were inappropriately elevated in water-loaded LTX-sheep (n = 3). Intracerebroventricular mannitol (1 ml/h for 2 h) resulted in a water diuresis and increase in CH 2O (-1.16 ± 0.12 to +2.81 ± 0.58 ml/min, P < 0.05) after 2 h in normal sheep, and plasma vasopressin levels fell significantly from to 0.88 ± 0.23 pg/ml to < 0.4 pg/ml (P < 0.05, n = 6). However, in LTX-sheep, there was no change in CH 2O (-1.31 ± 0.14 to -1.35 ± 0.12 ml/min) or the plasma vasopressin concentration (1.47 ± 0.18 to 1.60 ± 0.44 pg/ml, not significant) with i.c.v. mannitol. The results suggest that an inhibitory pathway from the vicinity of the median preoptic nucleus to the supraoptic and hypothalamic paraventricular nuclei plays an important role in the suppression of vasopressin secretion and the excretion of excess water., (© 2015 British Society for Neuroendocrinology.)

Few sex differences in regret or counterfactual thinking are evident in past research. The authors discovered a sex difference in regret that is both domain-specific (i.e., unique to romantic relationships) and interpretable within a convergence of theories of evolution and regulatory focus. Three studies showed that within romantic relationships, men emphasize regrets of inaction over action (which correspond to promotion vs. prevention goals, respectively), whereas women report regrets of inaction and action with equivalent frequency. Sex differences were not evident in other interpersonal regrets (friendship, parental, sibling interactions) and were not moderated by relationship status. Although the sex difference was evident in regrets centering on both sexual and nonsexual relationship aspects, it was substantially larger for sexual regrets. These findings underscore the utility of applying an evolutionary perspective to better understand goal-regulating, cognitive processes.

The lamina terminalis, located in the anterior wall of the third ventricle, is comprised of the subfornical organ, median preoptic nucleus (MnPO) and organum vasculosum of the lamina terminalis (OVLT). The subfornical organ and OVLT are two of the brain's circumventricular organs that lack the blood-brain barrier, and are therefore exposed to the ionic and hormonal environment of the systemic circulation. Previous investigations in sheep and rats show that this region of the brain has a crucial role in osmoregulatory vasopressin secretion and thirst. The effects of lesions of the lamina terminalis, studies of immediate-early gene expression and electrophysiological data show that all three regions of the lamina terminalis are involved in osmoregulation. There is considerable evidence that physiological osmoreceptors subserving vasopressin release are located in the dorsal cap region of the OVLT and possibly also around the periphery of the subfornical organ and in the MnPO. The circulating peptide hormones angiotensin II and relaxin also have access to peptide specific receptors (AT(1) and LGR7 receptors, respectively) in the subfornical organ and OVLT, and both angiotensin II and relaxin act on the subfornical organ to stimulate water drinking in the rat. Studies that combined neuroanatomical tracing and detection of c-fos expression in response to angiotensin II or relaxin suggest that both of these circulating peptides act on neurones within the dorsal cap of the OVLT and the periphery of the subfornical organ to stimulate vasopressin release.

Counterfactual thinking is associated with regulatory focus in a way that explains previous empirical incongruities, such as whether additive counterfactuals (mutations of inactions) occur more or less frequently than subtractive counterfactuals (mutations of actions). In Experiment 1, regulatory focus moderated this pattern, in that additive counterfactuals were activated by promotion failure, whereas subtractive counterfactuals were activated by prevention failure. In Experiment 2, additive counterfactuals evoked a promotion focus and expressed causal sufficiency, whereas subtractive counterfactuals evoked a prevention focus and expressed causal necessity. In Experiment 3, dejection activated additive counterfactuals, whereas agitation activated subtractive counterfactuals. These findings illuminate the interconnections among counterfactual thinking, motivation, and goals.

The effect of systemic or intracerebroventricular (ICV) infusion of the angiotensin AT1 receptor antagonist losartan on blood pressure during hypotensive haemorrhage was investigated in five conscious sheep. Mean arterial pressure (MAP) was measured during haemorrhage (15 mL kg-1 body wt). Losartan (1 or 0.33 mg h-1) was given to sheep by ICV, intravenous or intracarotid administration, beginning 60 min before and continuing during the haemorrhage. During control infusion of ICV artificial cerebrospinal fluid, MAP was maintained until 13.16 +/- 0.84 mL kg-1 blood loss, when a rapid reduction of at least 15 mmHg in arterial pressure occurred (the decompensation phase). ICV infusion of losartan at 1 mg h-1 caused an early onset of the decompensation phase after only 9.8 +/- 0.8 mL kg-1 of blood loss compared with control. Intravenous infusion of losartan (1 mg h-1) also caused an early onset (P < 0.05) of the decompensation phase at 10.2 +/- 1.0 mL kg-1 blood loss. This dose of losartan inhibited the pressor response to ICV angiotensin II, but not to intravenously administered angiotensin II, indicating that only central AT1 receptors were blocked. Bilateral carotid arterial administration of losartan at 0.33 mg h-1 caused an early onset of the decompensation phase during haemorrhage at 11.06 +/- 0.91 mL kg-1 blood loss (P < 0.05), which did not occur when infused by intravenous or ICV routes. The results indicate that an angiotensin AT1-receptor-mediated mechanism is involved in the maintenance of MAP during haemorrhage in sheep. The locus of this mechanism appears to be the brain.

1. Autoradiographic binding studies have shown that the AT(1) receptor is the predominant angiotensin II (AngII) receptor subtype in the central nervous system (CNS). Major sites of AT(1) receptors are the lamina terminalis, hypothalamic paraventricular nucleus, the lateral parabrachial nucleus, rostral and caudal ventrolateral medulla, nucleus of the solitary tract and the intermediolateral cell column of the thoraco-lumbar spinal cord. 2. While there are differences between species, AT(2) receptors are found mainly in the cerebellum, inferior olive and locus coeruleus of the rat. 3. Circulating AngII acts on AT(1) receptors in the subfornical organ and organum vasculosum of the lamina terminalis (OVLT) to stimulate neurons that may have a role in initiating water drinking. 4. Centrally administered AngII may act on AT(1) receptors in the median preoptic nucleus and elsewhere to induce drinking, sodium appetite, a sympathetic vasoconstrictor response and vasopressin secretion. 5. Recent evidence shows that centrally administered AT(1) antagonists inhibit dipsogenic, natriuretic, pressor and vasopressin secretory responses to intracerebroventricular infusion of hypertonic saline. This suggests that an angiotensinergic neural pathway has a role in osmoregulatory responses. 6. Central angiotensinergic pathways which include neural inputs to the rostral ventrolateral medulla may use AT(1) receptors and play a role in the function of sympathetic pathways maintaining arterial pressure., (1996 Blackwell Publishing Asia Pty Ltd.)

The effect of lowering cerebrospinal fluid (CSF) Na concentration on renal Na excretion (UNaV) was investigated in conscious sheep undergoing mineralocorticoid escape induced by intravenous infusion of aldosterone (20 micrograms.ml-1.h-1) for 3 days. On the 3rd day of aldosterone administration, when plasma and CSF Na concentration and mean arterial blood pressure (MABP) were increased as a result of the mineralocorticoid treatment, a reduction in the CSF Na concentration was induced by infusing a Na-free solution of 300 mmol/l mannitol (1 ml/h) into a lateral cerebral ventricle. This caused significant reductions in UNaV and MABP and a significant increase in renal free water clearance (CH2O). There was no significant change in glomerular filtration rate or plasma atrial natriuretic peptide concentration, but renal lithium clearance decreased. Simultaneous intravenous infusion of vasopressin (0.03 microgram/h) and lowering of CSF Na concentration also caused significant reductions in UNaV and MABP, but CH2O did not increase. We propose that increased Na concentration of brain fluid may initiate natriuretic and pressor mechanisms contributing to the process of mineralocorticoid escape. Reduced UNaV may have been due to reduced MABP, but it is unlikely to have been due to reduced plasma vasopressin levels.

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.