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

While we generally think of the brain and nervous system as central to most basic life processes, the concept of immune regulation or modulation is a relatively new idea. The novelty of such an association may be rooted in classic concepts of neurologic function describing direct innervation of controlled tissues and stimulation across synapses. The involvement of the neuroendocrine system in the precise control of metabolic and a variety of cellular functions should preface its involvement in defense against and/or surveillance for aberrant cell replication. Moreover, a principal characteristic of any control mechanism is feedback from the affected system (be it an organ or single cell). In this framework, it is not unreasonable to expect bidirectional interactions between the nervous and immune systems. Direct innervation of lymphoid tissues was described a number of years ago. More recently, immunoregulatory function has been demonstrated in vitro with a variety of neuroendocrine molecules such as the biogenic amines, SP, CGRP, SOM, vasopressin, ACTH, the endorphins, enkephalins, neurotensin, NGF and VIP. Now it has been shown that many of these same or similar neuroregulatory molecules are produced by cells of the immune system. The possibility that neurotransmitters or peptides, or both, may play a role in vivo in the maintenance of immunocompetence is supported by the finding that specific receptors for the neurohumoral modulators are present on the surface of immunocompetent cells. Current hypotheses speculate that feedback control mechanisms are manifested through the production of lymphokines, PGs and leukotrienes. Though it has not been possible to clearly demonstrate the reciprocal interaction between the neuroendocrine and immune systems in vivo, the evidence to date points to its inevitability.
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PMID:Neuroendocrine-immune interactions: immunoregulatory signals mediated by neurohumoral agents. 289 35

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

It has been previously shown that withdrawal from alcohol decreases the synthesis and expression of vasopressin (VP) and vasoactive intestinal polypeptide (VIP) in the suprachiasmatic nucleus (SCN), and that the infusion of NGF over 1 month completely restores these changes. Because SCN neurons do not express TrkA, NGF might have exerted its effects either through direct signalling of the neurons via p75NTR or by enhancing the activity of the cholinergic afferents to the SCN, which arise from the nucleus basalis magnocellularis (NBM). The observation that the infusion of NT-3 to withdrawn rats does not elicit any change in neuropeptide expression in the SCN suggests that ACh might be implicated in this process, a hypothesis that we have attempted to clarify in this study. For this purpose we destroyed, with quinolinic acid, the NBM of rats withdrawn from ethanol and later infused them with NGF over a period of 13 days. The total number and the somatic volume of SCN neurons immunoreactive for VP and VIP were stereologically estimated. No differences were found in the total number of neurons between quinolinic-injected NGF-treated withdrawn animals and intact withdrawn rats. However, the somatic volume of SCN neurons from quinolinic-injected animals was significantly reduced relative to control and withdrawn rats. The present results unequivocally demonstrate that the trophic effects exerted by NGF upon SCN neurons do not depend on direct neuronal signalling. Instead, they are indirect and, according to our results, NBM neurons, whose axons give rise to a cholinergic projection to the SCN, seem to be essential for eliciting those effects.
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PMID:The effects of nerve growth factor upon the neuropeptide content of the suprachiasmatic nucleus of rats withdrawn from ethanol are mediated by the nucleus basalis magnocellularis. 1552 May 30

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