1,721,245 research outputs found
Editorial: Dysmetabolism, obesity, and inflammation: Three prominent actors in the drama of major neuropsychiatric disorders
Full text linkVasopressin release to central and peripheral angiotensin II in rats with lesions of the subfornical organ
No full textAngiotensin II (Ang II), peripherally or centrally administered, increases plasma vasopressin concentrations in the rat. Peripherally injected Ang II was unable to effect the release of vasopressin in rats with subfornical organ (SFO) lesions. In contrast, a normal increase of plasma vasopressin levels was induced by centrally injected Ang II. These results suggest that peripherally administered Ang II elicits antidiuretic hormone (ADH) release by stimulating receptors in the SFO, whereas centrally administered Ang II acts at receptors outside the SFO. © 1984
[Efficacy of the oral treatment with L-tryptophan in subjects with insomnia. Preliminary results].
No full textEFFECT OF SUBSTANCES INFLUENCING BRAIN SEROTONERGIC TRANSMISSION ON PLASMA VASOPRESSIN LEVELS IN THE RAT
No full textStudies were carried out in the rat to investigate whether serotonin (5-HT) is involved in the regulation of vasopressin (ADH) release. For this purpose plasma ADH levels were measured in rats treated with drugs enhancing 5-HT transmission, such as d-fenfluramine and quipazine and with 5-HT depleting drugs, p-chlorophenylalanine (PCPA) and 5,7-dihydroxytryptamine (5,7-DHT). Forebrain 5HT, noradrenaline (NA) and dopamine (DA) were also measured. d-Fenfluramine and quipazine induced dose-related increases in plasma ADH levels in normohydrated rats. The effects of quipazine and d-fenfluramine were prevented by PCPA, indicating that 5-HT transmission was required for the biologic response. 5,7-DHT and PCPA pretreatment decreased forebrain 5-HT content and prevented ADH increases involved by water deprivation, suggesting that 5HT is necessary for the hormonal response to osmotic stimuli. The results summarized imply that serotonin may have a role in the physiological release of ADH from neuropophysis. © 1985
La neuroinfiammazione nel morbo di Alzheimer come target per nuove strategie terapeutiche.
No full textThirst and vasopressin secretion following central administration of angiotensin II in rats with lesions of the septal area and subfornical organ
No full textVarious dipsogenic stimuli, including peripheral and central administration of angiotensin II, have been shown to be capable of releasing vasopressin from the neurohypophyseal system. Studies were carried out in the rat to investigate whether the septal area, which contains a high concentration of angiotensin-sensitive cells and has neural connections with hypothalamic vasopressin-secreting neurons, mediated the stimulatory effect produced by angiotensin II on vasopressin release. Rats with electrolytic lesions in the region of the septal area had increased daily water consumption and urine output when these lesions included the medioventral or lateral nuclei of the septal forebrain, but not when the lesion involved the subfornical organ. No difference was observed in drinking responses following water deprivation or intracerebroventricular injection of angiotensin II in all experimental groups. In addition, the impaired ability to maintain water homeostasis (polyuro-polydipsic syndrome) of septal-lesioned rats was associated with decreased levels of circulating radioimmunoassayable vasopressin. Furthermore, the vasopressin release which occurred in response to intracerebroventricular angiotensin II in normal controls, shamlesioned and subfornical organ-lesioned rats was significantly attenuated in rats with electrolytic lesion of the medioventral or lateral septal area. Since cells in the lateral septal area are excited by iontophoretic application of angiotensin II, the present data might be consistent with the hypothesis that the stimulatory effect produced by central administration of angiotensin II on vasopressin release rests upon the integrity of the lateral septal area. © 1985
VASOPRESSIN RELEASE AFTER ENHANCED SEROTONERGIC TRANSMISSION IS NOT DUE TO ACTIVATION OF THE PERIPHERAL RENIN-ANGIOTENSIN SYSTEM
No full textPharmacological enhancement of 5-hydroxytryptamine (5-HT) transmission increases plasma vasopressin in rats. To investigate whether this effect is mediated through activation of the peripheral renin-angiotensin system, plasma vasopressin concentrations were measured after 5-HT activation in rats with lesions of the subfornical organ or pretreated with saralasin. The results show that the 5-HT-induced elevation of vasopressin is not due to activation of the peripheral renin-angiotensin system
CHOLINERGIC INPUTS TO THE MEDIAL SEPTAL NUCLEI OF THE RAT FOREBRAIN INCREASE PLASMA VASOPRESSIN LEVELS
No full textAstrocytes and the Psychiatric Sequelae of COVID-19: What We Learned from the Pandemic
Full text linkCOVID-19, initially regarded as specific lung disease, exhibits an extremely broad spectrum of symptoms. Extrapulmonary manifestations of the disease also include important neuropsychiatric symptoms with atypical characteristics. Are these disturbances linked to stress accompanying every systemic infection, or are due to specific neurobiological changes associated with COVID-19? Evidence accumulated so far indicates that the pathophysiology of COVID-19 is characterized by systemic inflammation, hypoxia resulting from respiratory failure, and neuroinflammation (either due to viral neurotropism or in response to cytokine storm), all affecting the brain. It is reasonable to hypothesize that all these events may initiate or worsen psychiatric and cognitive disorders. Damage to the brain triggers a specific type of reactive response mounted by neuroglia cells, in particular by astrocytes which are the homeostatic cell par excellence. Astrocytes undergo complex morphological, biochemical, and functional remodeling aimed at mobilizing the regenerative potential of the central nervous system. If the brain is not directly damaged, resolution of systemic pathology usually results in restoration of the physiological homeostatic status of neuroglial cells. The completeness and dynamics of this process in pathological conditions remain largely unknown. In a subset of patients, glial cells could fail to recover after infection thus promoting the onset and progression of COVID-19-related neuropsychiatric diseases. There is evidence from post-mortem examinations of the brains of COVID-19 patients of alterations in both astrocytes and microglia. In conclusion, COVID-19 activates a huge reactive response of glial cells, that physiologically act as the main controller of the inflammatory, protective and regenerative events. However, in some patients the restoration of glial physiological state does not occur, thus compromising glial function and ultimately resulting in homeostatic failure underlying a set of specific neuropsychiatric symptoms related to COVID-19
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