UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have shown previously that repeated restraint stress results in differential adaptation at both macrophysiological and cellular levels. Chronic stress accentuates vasopressinergic control of adrenocorticotropic hormone secretion in the pituitary. The present work determined whether endogenous vasopressin plays a role in response to repeated restraint. The first experiment explored changes in the response of repeatedly stressed animals to intracerebral vasopressin infusions. The second determined the effect of pretreating rats with a vasopressin V1a receptor antagonist on the way that they adapted to repeated restraint. Experiment 1: rats were subjected either to daily 60-min restraint for 10 days or transferred to the testing room where restraint sessions took place (controls). On the 11th day, they were infused with either artificial cerebrospinal fluid or 250 pmol vasopressin. The behavioural response to vasopressin was unaltered by previous stress. Plasma corticosterone was lowered in vasopressin-treated rats only after previous stress. Sixty minutes after vasopressin infusion, the central amygdala, locus coeruleus, the nucleus of the solitary tract and the dorsal vagal nucleus expressed increased levels of c-fos, and there were significant two-way interactions between stress and infusion for dorsal paraventricular nucleus, locus coeruleus and dorsal vagal nucleus. One-way analysis suggested that previous stress also reduced the c-fos response to vasopressin in the nucleus of the solitary tract. These results show that previous stress causes differential alterations in behavioural, endocrine and cellular responses to vasopressin. Experiment 2: rats were implanted with a transmitter which monitored heart rate and core temperature and a lateral cerebroventricular cannula. For 10 days, either artificial cerebrospinal fluid or 2500 pmol V1a antagonist, [d(CH2)1(5)-O-Me-Tyr2-Arg8]-vasopressin were infused i.c.v. 10 min prior to a 60-min restraint session. On the 11th day, no infusions were carried out, but rats received the usual period of restraint. The vasopressin antagonist was followed by motor responses (freezing, grooming and burrowing), more evident during the third and fifth days of stress. Core temperature responses were altered by the antagonist: stress-induced hypothermia was greatly reduced. Reduced baseline core temperatures, observed in controls as successive stress proceeded, were absent in antagonist-treated rats. By contrast, there were no significant effects of vasopressin antagonism on stress-induced tachycardia, nor in the way that this adapted to repeated restraint. On the 11th day (no i.c.v. infusions), hypothermic responses were no different in rats previously receiving either antagonist or control vehicle, but secondary hyperthermia was greater in the first group. Corticosterone levels were not altered by previous i.c.v. infusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in sensitivity to intracerebral vasopressin and the effects of a V1a receptor antagonist on cellular, autonomic and endocrine responses to repeated stress. 771 81

Intracerebroventricular (i.c.v.) infusions of neuropeptide Y (NPY) (2500 pmol) induced c-fos protein in the paraventricular nucleus (PVN) of intact male rats 60 min later. The greatest expression was observed in the dorsal (parvicellular) region of the PVN; there were intermediate levels in the lateral (magnocellular) and lowest ones in the medial (parvicellular) regions. Allowing rats to eat during the post-infusion interval did not modify this pattern of c-fos expression. Depriving rats of food for either 24 or 48 h did not induce recognisable expression of c-fos in the PVN, and allowing 24 h-deprived rats to eat also had no effect on PVN c-fos. Plasma insulin was increased by i.c.v. NPY, and raised still further in rats that were allowed to eat following NPY infusions. However, plasma glucose was not altered by either treatment. Food-deprived rats had low levels of insulin, but unaltered blood glucose, compared to controls. These results show that NPY can induce c-fos expression in both parvicellular and magnocellular areas of the PVN. The pattern of expression within the PVN seems to differ from that induced by other peptides, such as angiotensin II, vasopressin and corticotropin-releasing factor, suggesting that distinct populations of neurons are activated by different peptides within the complex structure of the PVN. Food deprivation does not induce c-fos expression within the PVN, though other studies have shown that NPY levels and release are both increased, so there is no simple relation between current energy state, blood levels of either glucose or insulin and c-fos expression within the PVN.
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PMID:c-fos expression in the paraventricular nucleus of the hypothalamus following intracerebroventricular infusions of neuropeptide Y. 771 25

There is evidence to indicate that cytokines of the interleukin series act within the brain to influence physiological responses to pathological states or stressful events. This investigation examined the effects of intracerebroventricular (lateral ventricle) injection of human recombinant interleukin-1 beta (IL-1 beta) on body temperature, hormone (catecholamine, cortisol, prolactin, growth hormone) release and hypothalamic expression of c-fos, corticotrophin-releasing hormone (CRH), vasopressin (AVP) and IL-1 beta mRNAs in the sheep. A preliminary study showed that central administration of 10 micrograms IL-1 beta significantly (P < 0.05) increased body temperature (by 1.2 degrees C) over a 140 min period but did not affect catecholamine secretion. A second experiment using graded doses (100 ng, 1 microgram, 10 micrograms) of IL-1 beta indicated that only the highest dose significantly (P < 0.01) increased cortisol concentrations and that none of the treatments altered the secretion of prolactin or growth hormone. In a third study, changes in gene expression in the hypothalamus were examined using in situ hybridization histochemistry following treatment with 10 micrograms IL-1 beta. The results showed that IL-1 beta increased c-fos mRNA in the paraventricular (PVN, P < 0.05) and supraoptic (SON, P < 0.05) nuclei, CRH mRNA in the PVN (P < 0.01) and IL-1 beta mRNA in the PVN (P < 0.05). There was, however, no change in AVP mRNA in either the PVN or the SON.
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PMID:Increased body temperature, cortisol secretion, and hypothalamic expression of c-fos, corticotrophin releasing hormone and interleukin-1 beta mRNAs, following central administration of interleukin-1 beta in the sheep. 777 2

c-fos expression mapping and electrophysiological recording experiments were done to clarify the role of the A1 noradrenergic cell group in the vasopressin response to hypotensive hemorrhage. In pentobarbital-anesthetized rats, moderate and severe hypotensive hemorrhages were simulated by brief occlusion of the inferior vena cava sufficient to reduce mean arterial pressure to approximately 50 or 30 mmHg, respectively. Both stimuli significantly increased the number of A1 region catecholamine cells displaying Fos-like immunoreactivity, this effect being most prominent at the level of the area postrema. Both stimuli also increased the number of supraoptic nucleus vasopressin cells displaying Fos-like immunoreactivity. Accordingly, electrophysiological studies involving separate animals confirmed that both moderate and severe caval occlusion significantly increased the firing of functionally identified vasopressin cells recorded in the supraoptic nucleus. However, although interruption of A1 region neuronal function by injection of gamma-aminobutyric acid at the level of the area postrema eliminated the increase in vasopressin cell firing elicited by moderate caval occlusion, it did not block the response to severe caval occlusion. These findings suggest that, in the rat, the vasopressin response to an acute reduction in central blood volume, such as that produced by hemorrhage, depends on the A1 projection only if the stimulus is of moderate intensity. Severe stimuli appear to involve activation of both the A1 projection and an additional vasopressin-stimulatory pathway that bypasses the A1 region.
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PMID:Rat vasopressin cell responses to simulated hemorrhage: stimulus-dependent role for A1 noradrenergic neurons. 777 99

Intracerebroventricular (i.c.v.) infusions of angiotensin II (AII) reliably induced c-fos expression in the supraoptic (SON) and paraventricular (PVN) nuclei, as well as other areas of the basal forebrain including the OVLT, subfornical organ (SFO), and bed nucleus (BNST). Double-labelling showed that AII-induced c-fos was observed in both vasopressin (AVP-) and oxytocin (OXY)-containing neurons of the SON and PVN in male rats. Allowing rats to drink water after AII infusions suppressed c-fos expression both AVP- and OXY-stained magnocellular neurons. Intragastric infusions of water were also effective, showing that oro-pharyngeal stimuli were not critical. Maximal suppression occurred in rats in whom water had been infused intragastrically about 5 min before i.c.v. AII infusions, suggesting that changes in osmolarity were responsible. i.c.v. AII also induced c-fos expression in a number of brainstem structures, including the solitary nucleus (NTS), lateral parabrachial nucleus (LPBN), locus coeruleus (LC), and the area postrema (AP). These results indicate that AVP and OXY-containing neurons in the magnocellular parts of the SON and PVN alter their immediate-early gene response to AII after water intake, and that this does not depend upon oro-pharyngeal factors. Furthermore, AII can induce c-fos expression in a number of brainstem nuclei associated with autonomic function, and these do not respond to water intake.
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PMID:Regional suppression by water intake of c-fos expression induced by intraventricular infusions of angiotensin II. 782 Jun 57

Previous neuropharmacological studies indicate that brain peptides are involved in mediating gastric stasis induced by abdominal surgery. Central pathways activated by abdominal surgery were investigated in the rat by using Fos protein as a marker of neuronal activation. Abdominal surgery (laparotomy alone or combined with cecal manipulation) was performed under brief enflurane anesthesia (7-8 minutes), and 1 hour later rats were killed and brains processed for Fos immunoreactivity. Double labeling with Fos and arginine vasopressin, oxytocin, or tyrosine hydroxylase antibodies was also performed. Abdominal surgery induced Fos staining in the nucleus tractus solitarii, paraventricular and supraoptic nuclei of the hypothalamus, locus coeruleus, and ventrolateral medulla. After abdominal surgery, 18-25% of vasopressin and 18-33% of oxytocin-labeled cells were found to be Fos positive in the paraventricular nucleus and 15% of activated cells in the nucleus tractus solitarii were positive for tyrosine hydroxylase immunoreactivity. Enflurane alone induced c-fos expression in the same brain area; however, the number of Fos-positive cells and double-labeled cells were decreased two- to fivefold and three- to eightfold, respectively, compared with the abdominal surgery groups. These data show that abdominal surgery induced activation of specific hypothalamic, pontine, and medullary neurons. These findings may have implications for the understanding of central mechanisms involved in mediating gastric ileus following abdominal surgery.
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PMID:Abdominal surgery induces Fos immunoreactivity in the rat brain. 786 Jul 79

The purpose of this study was to examine comprehensively and quantitatively the effects of sustained hypertension and hypotension on neuronal expression of Fos, the protein product of the proto-oncogene c-fos, in the brain of conscious rabbits. Hypertension or hypotension was produced by continuous intravenous infusion of phenylephrine or nitroprusside, at a rate sufficient to increase or decrease, respectively, arterial pressure by 20-30 mmHg, maintained for a period of 60 min. In comparison with a sham control group of rabbits that were infused with the vehicle solution alone, hypertension induced a significant increase in Fos immunoreactivity in the area postrema, the nucleus tractus solitarii, the caudal and intermediate ventrolateral medulla, the lateral parabrachial nucleus and the central nucleus of the amygdala. Double-labelling for tyrosine hydroxylase and Fos immunoreactivity showed that few (approximately 5%) of the Fos-positive neurons in the caudal and intermediate ventrolateral medulla in this group of animals were also positive for tyrosine hydroxylase. Hypotension also produced a significant increase in Fos immunoreactivity in the above regions, as well as in the rostral ventrolateral medulla, the A5 area, the locus coeruleus and subcoeruleus, the paraventricular nucleus, the supraoptic nucleus, the arcuate nucleus and the medial preoptic area. Approximately 65% of neurons in the rostral, intermediate and caudal ventrolateral medulla that expressed Fos following hypotension were also positive for tyrosine hydroxylase. Similarly, in the pons, approximately 75% of Fos-positive cells in the locus coeruleus, subcoeruleus and A5 area were positive for tyrosine hydroxylase. In the hypothalamus, 92% of Fos-positive neurons in the supraoptic nucleus, and 37% of Fos-positive neurons in the paraventricular nucleus, were immunoreactive for vasopressin. Our results demonstrate that hypertension and hypotension induce reproducible and specific patterns of Fos expression in the brainstem and forebrain. The distribution patterns and chemical characteristics of Fos-positive neurons following sustained hypertension or hypotension are significantly different. In particular, hypotension, but not hypertension, caused Fos expression in many tyrosine hydroxylase-positive cells within all pontomedullary catecholamine cell groups.
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PMID:Expression of Fos-like protein in brain following sustained hypertension and hypotension in conscious rabbits. 796 33

The effect of electrical stimulation of an important forebrain autonomic structure, the central nucleus of the amygdala (CNA), on c-fos expression in three hypothalamic nuclei was studied in rat with immunocytochemistry to reveal the protein (Fos) encoded by the immediate early gene (IEG). Image analysis was used to quantify the Fos immunoreactive neurons within the supraoptic (SON), paraventricular (PVN), and arcuate (AN) nuclei. Stimulation for 60 min induced a statistically significant increase of the number of Fos immunoreactive neurons in all three nuclei ipsilateral to the CNA stimulation site. Double immunocytochemical staining (Fos and vasopressin or Fos and oxytocin) was employed to evaluate the participation of different subpopulations of neurons within the SON and PVN in response to CNA stimulation. In the SON, the increased number of Fos immunoreactive nuclei following the stimulation was observed in the vasopressin and oxytocin-secreting cells within this nucleus. In the PVN, the increase in the number of Fos immunoreactive neurons was predominantly within the parvocellular compartment. These studies demonstrate that IEG expression in hypothalamic neurons can be evoked as a result of afferent stimulation from the CNA. Activation of peptide- and hormone-containing neurons within the SON, PVN and AN, through mono- or multisynaptic pathways, may play a role in hormonal and autonomic responses.
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PMID:Electrical stimulation of the central nucleus of the amygdala induces fos-like immunoreactivity in the hypothalamus of the rat: a quantitative study. 801 90

We have studied the induction of c-fos immunoreactivity (c-fos IR) in catecholaminergic and vasopressinergic immunoreactive neurons after repeated phosphate-buffered saline (PBS) loading or after repeated elicitation of the baroreceptor reflex via repeated infusion of the vasoconstrictor agent L-phenylephrine. About 75% and 30%, respectively, of the tyrosine-hydroxylase immunoreactive (IR) cell bodies of the ventral noradrenaline (NA) A1/adrenaline (A) C1 and dorsal NA A2/A C2 areas and 60% and 30%, respectively, of the phenylethanolamine N-methyltransferase IR nerve cells of the adrenaline C1 and C2 areas and 25% of the vasopressin (VP) IR neurons of the supraoptic (SO) nucleus developed nuclear c-fos IR after repeated PBS loading. This phenomenon remained unaltered by the repeated elicitation of the baroreceptor reflex. These results suggest that the activation of volume receptors promotes homeostatic responses via activation of early genes in subsets of central medullary noradrenaline and adrenaline neurons and SO VP neurons of the urethane-anaesthetized rat.
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PMID:Induction of c-fos immunoreactivity in tyrosine hydroxylase and phenylethanolamine-N-methyltransferase immunoreactive neurons of the medulla oblongata of the rat after phosphate-buffered saline load in the urethane-anaesthetized rat. 809 32

Intracerebroventricular (i.c.v.) injection of somatostatin (SS) or arginine-vasopressin (AVP) elicits barrel rotation (BR) in rats. To identify the potential neuron structures involved in this characteristic behavior, the regional expression of the c-fos gene in rat brain after i.c.v. injection of SS (10 micrograms) or AVP (1 micrograms) was examined by hybridization histochemistry. The c-fos expression could serve as a marker of neuronal activity and/or neural transmission. Following SS-induced BR, c-fos gene expression was observed in the lingula, uvula, nodulus, simplex, centralis, and culmen of the cerebellum, while following AVP-induced BR, c-fos gene expression was observed in the first four of the above-mentioned regions of the cerebellum, but not in the centralis or culmen. In these regions, the c-fos mRNA signals were observed on the granular layer. Expression of the c-fos gene was immediately and transiently induced and was not observed in rats in which BR was not evoked after SS or AVP injection. In both control rats and SS- or AVP-injected rats, the c-fos gene expression was induced in the piriform cortex and the flocculus of the cerebellum. The findings suggest that BR is a manifestation of behavior induced by massive transsynaptic activation of the granular cells in the cerebellum.
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PMID:Barrel rotation evoked by intracerebroventricular injection of somatostatin and arginine-vasopressin is accompanied by the induction of c-fos gene expression in the granular cells of rat cerebellum. 809 47

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