UNIPROT:Q86TM3 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early attempts to develop an animal model for anti-motion sickness drugs, using dogs and cats; were unsuccessful. Dogs did not show a beneficial effect of scopolamine (probably the best single anti-motion sickness drug for humans thus far) and the findings in cats were not definitive. The authors have developed an animal model using the squirrel monkey (Saimiri sciureus) of the Bolivian phenotype. Unrestrained monkeys in a small lucite cage were tested in an apparatus that induces motion sickness by combining vertical oscillation and horizontal rotation in a visually unrestricted laboratory environment. Signs of motion sickness were scored using a rating scale. Ten susceptible monkeys (weighing 800-1000 g) were given a total of five tests each, to establish the baseline susceptibility level. Based on the anticholinergic activity of scopolamine, the sensitivity of squirrel monkey to scopolamine was investigated, and the appropriate dose of scopolamine for this species was determined. Then various anti-motion sickness preparations were administered in subsequent tests: 100 ug scopolamine per monkey; 140 ug dexedrine; 50 ug scopolamine plus 70 ug dexedrine; 100 ug scopolamine plus 140 ug dexedrine; 3 mg promethazine; 3 mg promethazine plus 3 mg ephedrine. All these preparations were significantly effective in preventing motion sickness in the monkeys. Ephedrine, by itself, which is marginally effective in humans, was ineffective in the monkeys at the doses tried (0.3-6.0 mg). The squirrel monkey appears to be a good animal model for antimotion sickness drugs. Peripherally acting antihistamines such as astemizole and terfenadine were found to be ineffective, whereas flunarizine, and an arginine vasopressin V1 antagonist, showed significant activity in preventing motion sickness.
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PMID:Investigation of anti-motion sickness drugs in the squirrel monkey. 161 27

The effects of chronic (4 days) arginine vasopressin (AVP) infusion were studied in two separate groups of animals: normal Na-restricted dogs with intact renal nerves (n = 8) and renal-denervated Na-restricted dogs (n = 5). Volume expansion during AVP infusion was prevented in these studies with a sensitive servo-controlled cage-scale system. With intravenous AVP infusion (0.36 ng X kg-1 X min-1), plasma AVP levels increased from nearly 3 to 15 pg/ml, whereas total body weight remained unchanged from the control level. In renal-innervated dogs, plasma renin activity (PRA) decreased significantly (P less than 0.05) from control levels of 5.50 +/- 0.61 to an average level of 3.45 +/- 0.76 ng angiotensin I (ANG I) X ml-1 X h-1 on days 1 and 2 of AVP infusion. Thereafter, PRA tended to remain decreased on days 3 and 4, averaging 3.82 +/- 1.02 ng ANG I X ml-1 X h-1, but this was not statistically significant. Urinary Na excretion and balance, however, were not significantly altered during the 4-day AVP infusion period. In renal-denervated dogs, the rise of PRA with Na restriction was 50% that seen in normal dogs. In this group, a transient suppression of PRA was observed on day 1 of AVP infusion from 2.84 +/- 0.75 to 1.46 +/- 0.47 ng ANG I X ml-1 X h-1. Urinary Na excretion increased transiently with a small net Na loss of 4.9 +/- 1.3 meq on day 2 of AVP infusion. No significant changes occurred in average 24-h mean arterial pressure (MAP) in response to AVP in either group of dogs. Thus, in contrast to our previous observations in Na-replete dogs, elevations of plasma AVP within the physiological range result in suppression of PRA, but for periods of no longer than 1-2 days in Na-restricted dogs. This decrease of PRA occurred in the absence of measurable changes in MAP, total body weight, or plasma catecholamines. In addition, this transient AVP-induced suppression of PRA was only partially blunted by prior renal denervation. Finally, in the Na-restricted dog, AVP appears to have minimal or no long-term effects on urinary Na excretion.
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PMID:Chronic effects of vasopressin on plasma renin activity in sodium-restricted dogs. 351 20

The purpose of this study was to define the vasopressin-sensitive area in the anterior hypothalamus-medial preoptic area (AH-MPOA) of the golden hamster that is involved in the expression of flank-marking behavior. Male hamsters implanted with guide cannulae stereotaxically aimed at various sites in the AH-MPOA were microinjected initially with 0.1 ng of arginine vasopressin (AVP) in a volume of 10 nl. Hamsters that flank-marked in response to these injections were subsequently microinjected into the same sites with kainic acid (0.2 microgram/20 nl; n = 10) or an equal volume of 1 M NaOH as a vehicle control (n = 10). Four days later hamsters were tested for odor-induced flank marking by placing them into the recently vacated home cage of other hamsters and for flank marking in response to the microinjection of AVP. Animals treated with kainic acid exhibited significantly (p less than 0.01) fewer AVP and odor-induced flank marks as compared to the number of flank marks observed prior to treatment. There was no significant reduction in the number of flank marks in hamsters microinjected with the NaOH vehicle. In another group of hamsters, microinjection of kainic acid (0.2 microgram/20 nl) into the 3rd ventricle (n = 4) and other sites of the hypothalamus (n = 4) did not significantly alter odor-induced flank marking. The locations of the microinjection sites indicate that the neurons sensitive to AVP and involved in the expression of flank-marking behavior are found in the ventromedial area of the AH-MPOA extending from the caudal border of the suprachiasmatic nucleus to the rostral limit of the supraoptic nucleus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microinjection of kainic acid into the hypothalamus of golden hamsters prevents vasopressin-dependent flank-marking behavior. 378 73

Colchicine blockade of axonal transport from the paraventricular nucleus to the median eminence was used to indirectly infer ACTH secretagog release in response to the psychological stressors of social interactions and various degrees of novelty. Placing a rat in a new cage with either the smell or presence of a novel conspecific decreased arginine vasopressin and oxytocin (OT) contents, but not corticotropin-releasing factor content. Secretagog contents were unchanged in rats in their home cages faced with a novel conspecific. Secretagog release during social stress is thus primarily a function of being in a novel setting. For different degrees of novelty, rats were placed in either a novel cage, a novel bucket, or a novel bucket smelling of another rat. Whereas secretagog contents were unchanged with a novel cage, OT content alone decreased in response to both the bucket and the unclean bucket. Despite a graded corticosterone response, there was no distinction in the OT response, suggesting that the colchicine technique cannot accurately reflect gradations of stressors.
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PMID:Patterns of adrenocorticotropin secretagog release in response to social interactions and various degrees of novelty. 789 37

Reduction of renal mass (RRM) combined with a high-salt diet results in volume retention, a rise of cardiac output, and hypertension. The present studies were designed to determine whether prevention of volume retention would alter the rise of mean arterial pressure (MAP) in RRM rats given high salt. Rats were studied in a modified metabolic cage to permit continuous determination of total body weight (TBW). In group 1, NaCl was increased from 1 to 14.5 meq/day and delivered isotonically. In group 2, NaCl was increased while TBW was servo-controlled to a constant level. Group 3 was also servo-controlled, but rats received an intravenous infusion of an arginine vasopressin V1 antagonist throughout the study. MAP in group 1 rose 24 mmHg by day 4 of high salt with a parallel increase of TBW of 26 g. In group 2, MAP rose 48 mmHg by day 4 of high salt, while TBW was controlled to within 0.6% of control body weight. With inhibition of vasopressin V1 receptors (group 3), MAP rose 39 mmHg. Nearly equivalent amounts of NaCl were retained in all groups, which was associated with no change of plasma Na in group 1 but an increase of nearly 7 meq/ml in groups 2 and 3. Hematocrit fell nearly 9% in groups 2 and 3 compared with a 4% reduction in group 1. The results suggest that under conditions where net retention cannot occur, high salt intake increases MAP by an osmotically driven fluid transfer from cells, which results in an even greater expansion of blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension induced by high salt intake in absence of volume retention in reduced renal mass rats. 797 2

After intracerebroventricular (icv) injection of arginine-vasopressin (AVP; 0.1, 1, 3, 10, 30 and 100 ng) or artificial cerebrospinal fluid (aCSF), heart rate (HR), core temperature (CT), and gross activity were monitored by a wireless telemetry system in rats in the home cage for a 60-min period. In addition, the simultaneous occurrence of various behaviors was recorded by an observer. Also, two structurally related peptides, oxytocin (OXT) and desglycinamide-arginine vasopressin (DGAVP), were tested (10 and 100 ng). Both the time-effect and dose-response relationships of AVP-induced changes in HR and CT were biphasic. Lower doses of AVP produced a tachycardia, whereas injection of higher doses of AVP caused a tachycardia preceded by a significant bradycardia. The concomitant mild rise in CT seen in rats treated with 1 and 3 ng AVP or with aCSF was attenuated in rats given 10 ng AVP; 30 ng AVP resulted in an immediate significant fall in CT, which was restored to control values at 30 min after administration. An inverted U-shaped dose-response relationship was observed for gross activity, locomotion, and rearing behavior, whereas grooming behavior was most marked after the highest dose of AVP. OXT induced a grooming response and cardiac acceleration at the 100-ng dose only, whereas DGAVP produced no effect. To investigate the role of endogenous AVP in the maintenance of tonic ANS activity under resting conditions, rats were treated intracerebroventricularly (icv) with the V1 antagonist d(CH2)5-[Tyr(Me)2]AVP or polyclonal antiserum (W1E) against AVP. During the first 10 min after icv injection of 3 and 10 ng of the antagonist, an increase in HR, CT, and behavioral activation was observed, effects opposite to those produced by the higher dose of AVP. The same variables remained unchanged after administration of 100 ng of the antagonist. W1E injected icv was without effect. In summary, central effects of AVP on autonomic and behavioral activity seem to be mediated by differential neural pathways. In addition, a structure-activity relation seems to exist for the AVP-induced effects. Finally, these results suggest that AVP plays but a minor role in the maintenance of tonic activity of the ANS.
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PMID:Differential effects of centrally injected AVP on heart rate, core temperature, and behavior in rats. 843 Aug 86

In Syrian hamsters, arginine vasopressin (AVP) plays a critical role in the control of a form of scent marking called flank marking. Microinjection of AVP into the medial preoptic-anterior hypothalamus (MPOA-AH), lateral septal nucleus (LS), bed nucleus of the stria terminalis (BNST), and the periaqueductal gray (PAG) stimulates high levels of flank marking. Microinjection of an antagonist of the V1a-AVP receptor into sites such as the MPOA-AH inhibits expression of flank marking. The purpose of the present study was to investigate the neural circuit controlling flank marking by localizing the induction of Fos protein in response to the microinjection of AVP, a V1a-AVP antagonist (AVPA) or saline into the MPOA-AH. Immediately after microinjection, hamsters were placed in a clean cage and their behavior was videotaped for 10 minutes. Ninety minutes after the behavioral experiment hamsters were perfused and their brains removed for subsequent immunocytochemical localization of Fos protein. The number of Fos-positive neurons was significantly greater in the BNST, PAG, and central amygdala (Ce) following the microinjection of AVP than following the microinjection of either AVPA or saline. In AVP-injected animals, the number of Fos-labeled cells in the Ce, PVN, and PAG increased with increased frequency of either flank marking or flank gland grooming. These data support the hypothesis that neurons within the MPOA-AH, BNST, and PAG play an important role in the control of flank marking and suggest that the Ce may be a previously unrecognized part of this neural circuit.
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PMID:Neural circuitry controlling vasopressin-stimulated scent marking in Syrian hamsters (Mesocricetus auratus). 872 98

The effects of emotional stressors on the release of arginine vasopressin (AVP) and oxytocin (OXT) within the rat hypothalamus and the origin and physiological significance of AVP released within the hypothalamic paraventricular nucleus (PVN) were investigated. First, adult male Wistar rats with a microdialysis probe aimed at the PVN or the supraoptic nucleus were exposed to either a dominant male rat (social defeat) or a novel cage. Release of AVP within the PVN was significantly increased in response to social defeat but not to novelty. In contrast to an activation of the hypothalamic-pituitary-adrenal (HPA) system, neither stressor stimulated the hypothalamic-neurohypophysial system (unchanged plasma AVP and OXT and unchanged release within the supraoptic nucleus [AVP] and the PVN [OXT]). Next, we demonstrated by simultaneous microdialysis of the suprachiasmatic nucleus and the PVN that AVP measured in PVN dialysates during social defeat was probably of intranuclear origin. Finally, a mixture of a V1 AVP and the alpha-helical corticotropin-releasing hormone (CRH) receptor antagonists administered via inverse microdialysis into the PVN caused a significant increase in the plasma adrenocorticotropic hormone (ACTH) concentration compared with vehicle-treated controls both under basal conditions and during social defeat, indicating inhibitory effects of intra-PVN-released AVP and/or CRH on HPA system activity. The antagonists failed to affect anxiety-related behavior of the animals as assessed with the elevated plus-maze. Taken together, our results show for the first time that AVP is released within the PVN in response to an emotional stressor. We hypothesize that this intranuclear release provides a negative tonus on ACTH secretion.
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PMID:Release of vasopressin within the rat paraventricular nucleus in response to emotional stress: a novel mechanism of regulating adrenocorticotropic hormone secretion? 892 28

In the visible burrow system model of chronic social stress, male rats housed in mixed-sex groups quickly form a dominance hierarchy in which the subordinates appear to be severely stressed. A subgroup of subordinates have an impaired corticosterone response after presentation of a novel restraint stressor, leading to their designation as nonresponsive subordinates. To examine the mechanism underlying the blunted corticosterone response in these animals, in situ hybridization histochemistry was used to quantify corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) mRNA expression in the brain. In two separate visible burrow system experiments, the nonresponsive subordinates expressed a significantly lower average number of CRF mRNA grains per cell in the paraventricular hypothalamic nucleus compared with stress-responsive subordinates, dominants (DOM), or cage-housed control (CON) rats. The number of CRF mRNA labeled cells was also significantly lower in nonresponders than in responsive subordinates or DOM. In the central amygdala, CRF mRNA levels were increased in both groups of subordinates compared with CON rats, whereas responsive subordinates exhibited higher levels than the DOM rats as well. AVP mRNA levels did not vary with behavioral rank in any subdivision of the paraventricular hypothalamic nucleus. In the medial amygdala, the number of cells expressing AVP mRNA was significantly greater in CON rats compared with both groups of subordinates, although the average number of AVP mRNA grains per cell did not vary with rank. In addition, the number of AVP-positive cells significantly correlated with plasma testosterone level.
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PMID:Chronic social stress alters levels of corticotropin-releasing factor and arginine vasopressin mRNA in rat brain. 916 47

In adult rats, exposure to a novel environment, such as a simulated open field, elicits an increase in body core temperature. We have recently shown that this response is attenuated in midpregnancy and abolished at term of pregnancy in rats. We postulated that this gestation-dependent response resulted from alterations in the hypothalamic-pituitary-adrenal axis. To test this hypothesis, we measured the effects of pregnancy on renin, corticosterone, and arginine vasopressin (AVP) responses to exposure to either a simulated open field (30 or 120 min) or to the home cage (30 or 120 min) in rats. Pregnancy increased renin and corticosterone levels but not plasma AVP levels. Exposure to an open field decreased renin and increased plasma AVP levels in nonpregnant rats and on days 15 and 20 of gestation in pregnant rats, compared with home cage responses. Serum corticosterone levels were elevated after exposure to an open field in nonpregnant and pregnant rats, compared with home cage rats, the effect being more prolonged on day 20 of gestation. These observations provide new information on endocrine changes during pregnancy in rats and may help to explain the attenuated stress-induced hyperthermic response to exposure to a novel environment seen near term of pregnancy.
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PMID:Endocrine effects of pregnancy and exposure to a simulated open field in rats. 932 85

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