Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In situ hybridization and Northern blot assay were used to evaluate the effects of exogenous AVP(4-8) on the transcription of mRNAs for nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) in the adult rat brain. NGF and BDNF expression was found to be significantly enhanced by AVP(4-8) administration in the cerebral cortex and hippocampus, but NT-3 expression was not changed. In the same conditions, behavior-active arginine-vasopressin (AVP) showed a small effect and its behavior-inactive homologue, oxytocin did not. Our results suggest that selective regulation of neurotrophin gene expression by the peptides may be responsible for its memory-enhancing function.
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PMID:Facilitation of AVP(4-8) on gene expression of BDNF and NGF in rat brain. 939 59

Selective death of magnocellular vasopressinergic neurons in the hypothalamus has been reported in cases of hereditary and idiopathic diabetes insipidus and after experimental lesions of the hypothalamo-neurohypophyseal pathway. To identify trophic factors that promote survival of these neurons, an in vitro model system was established in which organotypic cultures of the rat hypothalamic paraventricular nucleus were maintained in chemically-defined medium. We observe that the majority of magnocellular vasopressinergic neurons die in these cultures, while other cell populations such as corticotrophin-releasing factor producing parvicellular and oxytocin producing magnocellular cells retain a well preserved cytoarchitectonic organization. Degenerating vasopressinergic cells exhibit morphological signs of apoptosis and stained positively when analysed by the terminal deoxynucleotidyl transferase biotinylated dUTP nick end-labelling assay. Partial survival of vasopressinergic neurons occurred after co-culturing the paraventricular nucleus with neurohypophyseal explants, indicating that target-derived factors may be required for the survival of these neurons. Cell survival is dramatically increased by the administration of ciliary neurotrophic factor and leukemia inhibiting factor, but not by interleukin 6 or the members of the neurotrophin family. Reverse transcription-polymerase chain reaction followed by Southern analysis shows the presence of ciliary neurotrophic factor messenger RNA in the neurohypophysis. Thus, endogenous ciliary neurotrophic factor and leukemia inhibiting factor, produced by neurohypophyseal cells may function as a physiological survival factor for neurosecretory vasopressinergic neurons.
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PMID:Magnocellular vasopressinergic neurons in explant cultures are rescued from cell death by ciliary neurotrophic factor and leukemia inhibiting factor. 975 24

The human supraoptic nucleus (SON) is the main production site of plasma vasopressin. Previously, using the Golgi apparatus and cell size as measures for neuronal metabolic activity, an activation of vasopressinergic neurons was found during ageing in the human SON in women but not in men. We hypothesized that the low-affinity neurotrophin receptor p75 (p75(NTR)) might be involved in the mechanism of activation of vasopressin neurons in postmenopausal women, since this receptor was found to be expressed in the SON neurons of aged individuals, and because p75(NTR) expression was shown to be suppressed by estrogens. Therefore, we investigated whether p75(NTR) immunoreactivity in the SON neurons was age- and sex-dependent. For this purpose, we studied paraffin sections of the SON in 32 postmortem brains of control patients ranging in age from 29 to 94 years with an anti-p75(NTR) antibody and determined the area of p75(NTR) immunoreactivity per neuron using an image analysis system. To study whether the p75(NTR) might also participate in the activation of SON neurons, we related Golgi apparatus size to the area of p75(NTR) immunoreactivity per cell in the same patients. We found that the area of p75(NTR) immunoreactivity per cell correlated indeed significantly with age and with Golgi apparatus size only in women but not in men. Therefore, our results suggest that p75(NTR) is involved in postmenopausal activation of vasopressinergic neurons in the human SON.
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PMID:Sex- and age-related P75 neurotrophin receptor expression in the human supraoptic nucleus. 1077 44

Activity of magnocellular vasopressin (VP) neurons in the human hypothalamus is sex- and age-dependent as judged from the size of the Golgi apparatus, neuronal size and VP mRNA levels. These parameters are significantly higher in young (< or = 50 years old) men than in young women and are markedly increased in postmenopausal women compared to premenopausal women. This data suggest an inhibitory effect of estrogens on metabolic activity of VP neurons in the human supraoptic nucleus (2SON), which is likely to be mediated via estrogen receptor (ER) beta. Estrogens were shown to mediate their inhibitory effect via ER beta. It is expressed to a much higher degree in the SON of young women than in other groups, whereas estrogen receptor alpha, that mediates stimulatory effects of estrogens, is present in a small proportion of SON neurons. In addition, estrogens inhibit p75 neurotrophin receptor expression in VP cells. In conclusion, we discuss the inhibitory role of estrogens in functional activity of human VP neurons, which is most probably mediated directly via ER beta and indirectly by p75 neurotrophin receptor.
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PMID:[Activity of vasopressin neurons in the human supraoptic nucleus: estrogen inhibitory effect]. 1123 35

We have shown that osmotic stress increases brain-derived neurotrophic factor (BDNF) mRNA in the supraoptic nucleus and that this increase seems to be determined by the high expression of transcripts containing exon I. The paraventricular nucleus is another hypothalamic neuronal subset where BDNF mRNA is also sensitive to osmotic stress stimulation. In this nucleus, transcripts containing exon I were not modified but only those containing exon II. By contrast, transcripts containing exon III did not exhibit any variation in our experimental conditions. The presence of BDNF mRNA in both paraventricular and supraoptic hypothalamic nuclei was recently reported. These nuclei are extremely sensitive to osmotic stimuli and their neurons secrete oxytocin and arginine-vasopressin in the posterior pituitary gland. This study was thus designed to investigate the possible involvement of BDNF in the response of supraoptic nucleus to osmotic stress stimulus. Osmotic stress was induced by hypertonic saline injection (1.35% NaCl) administered to animals 3 h before analysis. We used non-isotopic in situ hybridization to study the expression of BDNF mRNA and its transcripts with antisense riboprobes on histological brain sections, including paraventricular and supraoptic nuclei from control and osmotic stress-stimulated animals. To investigate a possible correlation between the expression of BDNF mRNA and arginine-vasopressin, the peptide content was analyzed by immunohistochemistry in both paraventricular and supraoptic nuclei at two different times after hyperosmotic injection. The results showed that BDNF mRNA expression preceded the arginine-vasopressin increase. In addition, on serial adjacent histological sections of supraoptic nucleus (10 microm), both BDNF and arginine-vasopressin mRNAs were visualized by isotopic in situ hybridization and the images were overlaid, showing that almost all of the hybridization signals were overlapped. Taken together our results are in keeping with the hypothesis that activation of the different BDNF promoters seems to be region-specific. Besides, the temporal correlation between both BDNF mRNA expression and arginine-vasopressin content, as well as the morphological vicinity between their respective producing cells in the supraoptic nucleus, suggest an autocrine or paracrine action for this neurotrophin in the regulation of arginine-vasopressin secretion.
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PMID:Osmotic stress increases brain-derived neurotrophic factor messenger RNA expression in the hypothalamic supraoptic nucleus with differential regulation of its transcripts. Relation to arginine-vasopressin content. 1208 43

Some neurotrophins have the capability of enhancing neuropeptide expression in several regions of the brain. It was also recently shown that NGF, infused over 1 month, offsets the decreased synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN) of rats submitted to chronic ethanol treatment and withdrawal. In the present study we examined the effectiveness of neutrotrophin-3 (NT-3) in promoting such effects, given that SCN neurons express both the high and the low affinity receptors for this neurotrophin. NT-3 was intraventricularly infused during 10 days to rats withdrawn from prolonged ethanol treatment. The total number, and the mean somatic volume, of VP- and VIP-immunoreactive neurons was compared with the estimates obtained from control rats and withdrawn rats treated with either NGF or cerebrospinal fluid during the same period. The infusion of cerebrospinal fluid and of NT-3 did not prevent the reduction in the number of peptide-producing neurons induced by withdrawal from ethanol treatment. Conversely, NGF infusion increased their number to control levels and led to neuronal hypertrophy. Our results show that, unlike NGF, NT-3 does not display the capacity of enhancing neuropeptide expression in the SCN. Because SCN neurons express the low affinity p75(NTR), which is equally activated by both neurotrophins, our results additionally indicate that the effects of NGF upon SCN neurons are not receptor-mediated. Taken together, our data suggest that indirect mechanisms, rather than direct neutrophin signaling, are likely to mediate the trophic effects exerted by NGF upon SCN neurons.
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PMID:NGF and NT-3 exert differential effects on the expression of neuropeptides in the suprachiasmatic nucleus of rats withdrawn from ethanol treatment. 1291 67

Brain-derived neurotrophic factor is a neurotrophin belonging to the nerve growth factor family, which is involved in the differentiation and survival of many types of neurons. It also participates in neuroprotection and neuronal plasticity in adult rats. Our previous studies showed that a single brain-derived neurotrophic factor injection modifies hypothalamic-pituitary-adrenal axis activity in adult male rats. To investigate the effect of chronic brain-derived neurotrophic factor administration on some physiological parameters, adult rats were implanted with osmotic micro-pumps to deliver brain-derived neurotrophic factor continuously for 14 days in the lateral ventricle (12 microg/day/rat). mRNA levels were evaluated by in situ hybridization analysis, peptide contents and plasma hormone concentrations by radioimmunoassay. Animals were also equipped with telemetric transmitters to study locomotor activity and temperature rhythms modifications, since hypothalamic-pituitary-adrenal axis is known to modulate these two parameters. Decreased body weight was used as a control of brain-derived neurotrophic factor access to hypothalamic areas as already documented. In the hypothalamus the continuous brain-derived neurotrophic factor treatment increases: (i) the mRNA steady state levels of corticotropin releasing hormone and arginin-vasopressin in the paraventricular nucleus, the supraoptic nucleus, and the suprachiasmatic nucleus; (ii) the surface of corticotropin releasing hormone and arginin-vasopressin mRNA signals in these nuclei as detected by in situ hybridization, and (iii) the corticotropin releasing hormone and arginin-vasopressin contents. The plasma concentrations of adrenocorticotropic hormone and corticosterone were decreased and increased, respectively. Finally, this treatment increased daily locomotor activity and temperature, and provoked some circadian perturbations. These results obtained after chronic brain-derived neurotrophic factor administration extend data on the brain-derived neurotrophic factor involvement in the hypothalamic-pituitary-adrenal axis regulation and illustrate its effects on the locomotor and temperature rhythms. They also allow demonstrating that the regulation of the hypothalamic-pituitary-adrenal axis by brain-derived neurotrophic factor differs according to the brain-derived neurotrophic factor administration mode, i.e. acute injection or chronic administration.
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PMID:Continuous i.c.v. infusion of brain-derived neurotrophic factor modifies hypothalamic-pituitary-adrenal axis activity, locomotor activity and body temperature rhythms in adult male rats. 1645 53

In vitro experiments demonstrated the neuroprotective effect of dipeptide pGlu-Asn-NH2, which corresponded to the N-terminal fragment of the major vasopressin metabolite AVP(4-9). The dipeptide in concentrations of 10(-5)-10(-7) M prevented death of HT-22 immortalized hippocampal neurons under conditions of oxidative stress and protected PC-12 rat pheochromocytoma cells from neurotoxic compound 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. pGlu-Asn-NH2 in a concentration of 10(-6) M increased the content of endogenous neuroprotective substances, neurotrophin NGF and heat shock protein HSP70 in HT-22 cells. Our results indicate that this dipeptide can be used for the therapy of Parkinson's disease.
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PMID:Neuroprotective effect of dipeptide AVP(4-5)-NH2 is associated with nerve growth factor and heat shock protein HSP70. 1864 9

Throughout literature--fiction and poetry, fine arts and music--falling in love and enjoying romantic love plays a central role. While several psychosocial conceptions of pair attachment consider the participation of hormones, human endocrinology has dealt with this theme only marginally. According to some authors in addictology, falling in love shows some signs of hormonal response to stressors with changes in dopamine and serotonin signalling and neurotrophin (transforming growth factor b) concentration. Endorphins, oxytocin and vasopressin may play a role during the later phases of love. However, proof of hormonal events associated with love in humans has, until recently, been lacking.
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PMID:Endocrine factors of pair bonding. 1878 Jun 41

The mechanisms by which dietary salt promotes hypertension are unknown. Previous work established that plasma [Na(+)] and osmolality rise in proportion with salt intake and thus promote release of vasopressin (VP) from the neurohypophysis. Although high levels of circulating VP can increase blood pressure, this effect is normally prevented by a potent GABAergic inhibition of VP neurons by aortic baroreceptors. Here we show that chronic high salt intake impairs baroreceptor inhibition of rat VP neurons through a brain-derived neurotrophic factor (BDNF)-dependent activation of TrkB receptors and downregulation of KCC2 expression, which prevents inhibitory GABAergic signaling. We show that high salt intake increases the spontaneous firing rate of VP neurons in vivo and that circulating VP contributes significantly to the elevation of arterial pressure under these conditions. These results provide the first demonstration that dietary salt can affect blood pressure through neurotrophin-induced plasticity in a central homeostatic circuit.
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PMID:High salt intake increases blood pressure via BDNF-mediated downregulation of KCC2 and impaired baroreflex inhibition of vasopressin neurons. 2586 41


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