Publications by authors named "Wied D"

Familial neurohypophysial diabetes insipidus (FNDI) is caused by a defect in vasopressin synthesis and release as a result of a heterozygous mutation in the gene for the vasopressin prohormone. The predominant characteristic of FNDI is excessive thirst and urine production. However, vasopressin not only has peripheral endocrine effects, but also regulates numerous brain functions.

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The present review summarizes the findings on the role of neuropeptides in the pathophysiology of schizophrenia and major depression. Several neuropeptides as vasopressin and endorphins in particular, beta-endorphin and gamma-type endorphins, cholecystokinin (CCK), neurotensin, somatostatin and Neuropeptide Y have been implicated in schizophrenia. During the last decade, however, few attempts to explore the significance of most of these and other neuropeptides in the pathophysiology of the disease or their therapeutic potential are found in the literature.

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Energy homeostasis is controlled by a complex neuroendocrine system consisting of peripheral signals like leptin and central signals, in particular, neuropeptides. Several neuropeptides with anorexigenic (POMC, CART, and CRH) as well as orexigenic (NPY, AgRP, and MCH) actions are involved in this complex (partly redundant) controlling system. Starvation as well as overfeeding lead to changes in expression levels of these neuropeptides, which act downstream of leptin, resulting in a physiological response.

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Familial neurohypophysial diabetes insipidus (FNDI) is an autosomal dominant trait in which expression of a mutant vasopressin prohormone reduces vasopressin production. We investigated the NP85 Cys-->Gly mutant vasopressin prohormone in a large kindred in The Netherlands. We demonstrate that growth retardation is an important early sign in two children from this kindred, which recuperates by substitution therapy with 1-desamino-8-D-arginine vasopressin.

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Earlier work has shown that plasma vasopressin levels of depressed patients were higher than those of healthy controls. The aim of the present study was to determine whether plasma vasopressin levels were correlated to parameters of the circadian rhythm. Forty-one patients with major depression and twenty-five controls participated in a case-control design under natural circumstances in a field study to investigate plasma vasopressin levels three times daily, circadian motor activity, and the 24-h periodicity of body temperature for five consecutive 24-h periods.

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The bed nucleus of the stria terminalis (BNST) is involved in autonomic and behavioral reactions to fearful stimuli and contains corticotropin-releasing hormone (CRH) fibers and terminals. The role of CRH in the medial part of the BNST in the regulation of heart rate (HR) and PQ interval of the electrocardiogram was studied under resting conditions and conditioned fear stress in freely moving rats. Microinfusion of CRH (0.

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The involvement of the corticotropin-releasing hormone (CRH) type 1 receptor in CRH-induced cardiac responses was studied in freely moving rats. Intracerebroventricular (icv) infusion of 2 microg CRH under resting conditions resulted in a significant increase in heart rate (HR), but did not significantly affect the PQ interval of the electrocardiogram. This effect involves sympathetic nervous system (SNS) activation, since CRH-treatment resulted in a marked increase in plasma norepinephrine (NE) and epinephrine (E), and sympathetic blockade by subcutaneously injected atenolol (1 mg/kg), a beta1-selective adrenergic antagonist, completely prevented the CRH-induced tachycardia.

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The role of the endogenous corticotropin-releasing hormone (CRH) system in the regulation of heart rate, PQ interval (a measure of vagal activity), gross activity and release of adrenocorticotropic hormone (ACTH), noradrenaline and adrenaline into the blood during conditioned fear was studied in freely moving rats. Intracerebroventricular (i.c.

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Neuropeptides are peptides which affect the nervous system. They are derived from large precursor molecules. These are converted to neurohormones, neuropeptides of the "first generation", which can be further converted to neuropeptides of the "second generation".

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Behavioral neuroscience is using more and more gene knockout techniques to produce animals with a specific deletion. These studies have their precedent in nature. A mutation may result in a limited genetic defect, as seen in the vasopressin (VP) deficiency in the Brattleboro rat.

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The effects of endogenous metabolites of the neuropeptide vasopressin (VP) in behavioural tests led to the hypothesis that VP metabolites have a more selective function than VP. In contrast to VP, no peripheral effects have been found thus far with VP metabolites and their function seems to be associated with memory-related behaviour. VP metabolites can improve both consolidation and retrieval of memory.

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The effects of conditioned fear on gross activity, heart rate, PQ interval, noradrenaline and adrenaline were studied in freely moving rats. Subcutaneous (s.c.

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Background: The aim of the study was to search for the existence of, and define, a possible relationship between performance in neuropsychological tests and baseline concentrations of plasma cortisol, vasopressin and oxytocin in medication-free patients with a major depressive episode.

Methods: Measures of depression and anxiety were obtained and a neuropsychological battery was presented. Blood for neuropeptide analysis was drawn by venepuncture at 8.

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Background: Previously, we found that mean plasma concentrations of arginine vasopressin (AVP), but not of oxytocin (OT), were higher in depressed patients than in healthy controls. Plasma AVP concentrations were positively correlated to clinically rated psychomotor retardation. To further explore this previously reported relation we studied psychomotor retardation by means of an activity monitor, which is a more fine-focused and more objective instrument to analyze motor retardation than a clinical rating scale.

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The effects of repeated exposure to a novel test box on cardiac and behavioral activities (locomotion, rearing, grooming, scanning, and immobility) were studied in rats tested during the dark phase ("dark" rats) or the light phase ("light" rats) of the lighting cycle, using a telemetry system for registration of ECGs during the first and fifth tests. Heart rate (HR) was used to monitor sympathetic and parasympathetic activity; the PQ interval was used to monitor parasympathetic activity. Behavior was videotaped simultaneously.

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The hole board search task (HBST) measures long-term and short-term memory, operationally defined as reference memory and working memory. The HBST is an open-field spatial learning test. Previously, we have shown that desglycinamide(Arg8) vasopressin (DGAVP) modulated reference memory, working memory, spatial sequence memory, and learning in the HBST in a dose-dependent manner (Vawter MP, Van Ree JM.

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Mentally healthy subjects show increased plasma concentrations of the neuropeptides, arginine vasopressin (AVP) and oxytocin (OT), under conditions of stress, but data are lacking about plasma concentrations of AVP and OT in patients with major depression. We thus assessed plasma concentrations of AVP and OT in patients with major depression (n = 52) and healthy controls (n = 37). Mean plasma AVP concentrations were higher in the group of depressed patients than in controls.

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Subcutaneously (s.c.) administered [Arg8]vasopressin (AVP) potentiated seizures induced by intracerebroventricular (i.

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The central opioid system may have an important influence on memory processes. In view of this, the concentration of beta-endorphin-like immunoreactivity (beta-ELIR) in cerebrospinal fluid (CSF) was measured by a radioimmunoassay in rats trained in a passive avoidance procedure. The beta-ELIR in CSF was examined immediately, 2, 5, 10, and 30 min after the learning trial in which rats were exposed to footshock (0, 0.

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Vasopressin (VP) is axonally distributed in many brain structures, including the ventral hippocampus. Picogram quantities of VP injected into the hippocampus improve the passive avoidance response of rats, presumably by enhancing memory processes. Vasopressin is metabolized by the brain tissue into shorter peptides, such as [pGlu4,Cyt6]VP(4-9) and [pGlu4,Cyt6]VP(4-8), which preserve the behavioral activity but lose the peripheral activities of the parent hormone.

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