Arginine vasopressin in the caudate nucleus plays an antinociceptive role in the rat

Our previous work has shown that arginine vasopressin (AVP) regulates antinociception through brain nuclei rather than the spinal cord and peripheral organs. The present study investigated the nociceptive effect of AVP in the caudate nucleus (CdN) of the rat. Microinjection of AVP into the CdN increased pain threshold in a dose-dependent manner, while local administration of AVP-receptor antagonist-d(CH(2))(5)Tyr(Et)DAVP decreased pain threshold. Pain stimulation elevated AVP concentration in CdN perfuse liquid. CdN pretreatment with AVP-receptor antagonist completely reversed AVP's effect on pain threshold in the CdN. The data suggest that AVP in the CdN is involved in antinociception.     

Arginine vasopressin causes morphological changes suggestive of fluid transport in rat choroid plexus epithelium

Summary The experiments described herein use an in vitro preparation of choroid plexus to demonstrate that it is a vasopressin-responsive organ by morphologic criteria. Choroid plexus from rats was incubated for one hour in graded concentrations of arginine vasopressin (AVP). Within physiologic range of molar concentration, incubation in vasopressin induced a decrease in basal and lateral spaces in choroid plexus epithelial cells as well as an increase in number of dark cells. The number of cells with basal spaces decreased significantly from 82.7±9.2 in control tissue to 19±18 in tissue incubated in 10^-12 M AVP; similarly, the number with lateral cellular spaces decreased from 20±8.8 to 7.6±2.2 cells in 10^-10 M AVP. Dark cells increased in number from 3.8±2.6 in control conditions to 49±4 with 10^-9 M vasopressin. These data suggest important effects of arginine vasopressin in cerebrospinal fluid (CSF) on choroid plexus, compatible with enhanced fluid transport across choroid epithelial cells.     

Supplemental ascorbic acid does not affect inferred heat loss in broiler chickens exposed to elevated temperature

The provision of supplemental ascorbic acid has been reported to lower the body temperature of chickens maintained at elevated environmental temperatures. Since body temperature is the net effect of heat production and heat loss, it is not known if the reductions in body temperature were due to a lower heat production or an increase in heat loss. The purpose of this work was to determine if supplemental ascorbic acid facilitates heat loss in chickens exposed to an elevated temperature. On day 12 post-hatch broiler chickens were implanted intra-abdominally with a thermo-sensitive radio transmitter. The following day, birds were placed inside an indirect calorimeter maintained at 34 C for 24 h and provided water containing 0 or 400 ppm ascorbic acid. Oxygen consumption, carbon dioxide production, heat production, respiratory exchange ratio, and body core temperature were measured for 3 h; beginning 21 h after the birds were placed inside the calorimeter. No differences were observed in heat production or body core temperature between birds provided or not and 400 ppm ascorbic acid. This suggests that ascorbic acid has no effect on heat loss. Birds provided ascorbic acid did exhibit a significantly lower respiratory exchange ratio suggesting a greater utilization of lipid for energy production. Although lipid has a lower heat increment compared with protein and carbohydrate, the significance of this finding to birds exposed to elevated temperature is not known. In conclusion, under the conditions of this study the provision of supplemental ascorbic acid to broiler chickens maintained at an elevated temperature did not affect heat loss as inferred from measured heat production and body core temperature.     

Arginine vasopressin in fever: a still unsolved puzzle

(1) Administration of arginine vasopressin (AVP) in the ventral septal area (VSA) or intracerebroventricularly (i.c.v.) is thought to attenuate lipopolysaccharide (LPS) or prostaglandin (PG) E₂ fevers in rabbits and rats by acting on the V₁ receptor. (2) We found that the fever response of rabbits to intravenous LPS (200 ng/kg) or intra-VSA PGE₂ (500 ng) was not attenuated but enhanced by intra-VSA AVP (5 μg); a pharmacological analysis showed that this fever-enhancing effect was mediated by the V₂ receptor. (3) The febrile response of rats to intraperitoneal (50 μg/kg) or i.c.v. (100 ng) LPS was unaffected by i.c.v. AVP (2.5–100 ng). (4) The role of AVP in fever should be re-examined.     

Arginine vasopressin improves the memory deficits in Han Chinese patients with first-episode schizophrenia

The memory impairment is a core deficit in the first-episode schizophrenia patients. Arginine vasopressin (AVP) in the brain can improve learning and memory. We performed multicentre, randomized, double-blind, placebo-controlled, parallel-group clinical trial to study the cognitive functioning in Han Chinese first-episode schizophrenic patients in a 12-week treatment regime with the intranasal administration of AVP (128 cases) or placebo (131 cases) in addition to the conventional treatment. The methods of positive and negative syndrome scale (PANSS), Wechsler memory scale-4th edition (WMS-IV) and event-related potential (ERP) were used to study the effects of AVP on the cognitive function. The results showed that (1) AVP concentration decreased in cerebrospinal fluid (CSF) of the right-handed Han Chinese first-episode schizophrenic patients comparing with that of the health volunteers (7.1 ± 1.5 pg/ml vs 13.3 ± 1.9 pg/ml, p < 0.01), and did not change in plasma; (2) AVP significantly improved PANSS scores including total scores, positive symptoms, negative symptoms and general psychopathology comparing with those of the placebo group; (3) AVP elevated WMS-IV scores including the long-term memory (accumulation), short-term memory (recognition, comprehension), immediate memory (number recitation) and memory quotient 4, 8 and 12 weeks after treatment; and (4) AVP did not influence the latency and wave amplitude of target stimulus of P₃₀₀ of right-handed Han Chinese first-episode schizophrenic patients. The data suggested that AVP might improve cognitive process, such as memorizing and extraction of the information although there were many changes of cognitive functions in the right-handed Han Chinese first-episode schizophrenic patients.     

Arginine vasopressin in hypothalamic paraventricular nucleus is transferred to the caudate nucleus to participate in pain modulation

Arginine vasopressin (AVP), which is synthesized and secreted in the hypothalamic paraventricular nucleus (PVN), is the most important bioactive substance in the pain modulation. Our pervious study had shown that AVP plays an important role in pain modulation in caudate nucleus (CdN). The experiment was designed to investigate the source of AVP in CdN by the nucleus push-pull perfusion and radioimmunoassay. The results showed that: (1) pain stimulation increased the AVP concentration in the CdN perfusion liquid, (2) PVN decreased the effect of pain stimulation which was stronger in both sides than in one side of PVN cauterization; and (3) L-glutamate sodium would excited the PVN neurons by the PVN microinjection that could increase the AVP concentration in the CdN perfusion liquid. The data suggested that AVP in the CdN might come from the PVN in the pain process, i.e., AVP in the PVN might be transferred to the CdN to participate in the pain modulation.     

Arginine vasopressin in hypothalamic paraventricular nucleus is transferred to the nucleus raphe magnus to participate in pain modulation

Hypothalamic paraventricular nucleus (PVN) is one of the main sources of arginine vasopressin (AVP) synthesis and secretion. AVP is the most important bioactive substance in PVN regulating pain process. Our pervious study has pointed that pain stimulation induced AVP increase in the nucleus raphe magnus (NRM), which plays a role in pain modulation. The present study was designed to investigate the source of AVP in the rat NRM during pain process using the methods of nucleus push–pull perfusion and radioimmunoassay. The results showed that pain stimulation increased the AVP concentration in the NRM perfusion liquid, PVN cauterization inhibited the role that pain stimulation induced the increase of AVP concentration in the NRM perfusion liquid, and PVN microinjection of l-glutamate sodium, which excited the PVN neurons, could increase the AVP concentration in the NRM perfusion liquid. The data suggested that AVP in the PVN might be transferred to the NRM to participate in pain modulation.     

Oxytocin, but not arginine vasopressin is involving in the antinociceptive role of hypothalamic supraoptic nucleus

Our pervious study has demonstrated that the hypothalamic supraoptic nucleus (SON) plays a role in pain modulation. Oxytocin (OXT) and arginine vasopressin (AVP) are the important hormones synthesized and secreted by the SON. The experiment was designed to investigate which hormone was relating with the antinociceptive role of the SON in the rat. The results showed that (1) microinjection of l-glutamate sodium into the SON increased OXT and AVP concentrations in the SON perfusion liquid, (2) pain stimulation induces OXT, but not AVP release in the SON, and (3) intraventricular injection (pre-treatment) with OXT antiserum could inhibit the pain threshold increase induced by SON injection of l-glutamate sodium, but administration of AVP antiserum did not influence the antinociceptive role of SON stimulation. The data suggested that the antinociceptive role of the SON relates to OXT rather than AVP.     

Only through the brain nuclei, arginine vasopressin regulates antinociception in the rat

The effect of arginine vasopressin (AVP) on rat antinociception was investigated. Intraventricular injection of 50 or 100 ng AVP dose-dependently increased the pain threshold; in contrast, intraventricular injection of 10 μl anti-AVP serum decreased the pain threshold; both intrathecal injection of 200 ng AVP or 10 μl anti-AVP serum and intravenous injection of 5 μg AVP or 200 μl anti-AVP serum did not influence the pain threshold. Pain stimulation reduced AVP concentration in hypothalamic paraventricular nucleus (PVN), and elevated AVP concentration in hypothalamic supraoptical nucleus (SON) and periaqueductal gray (PAG), but no change in AVP concentration was detected in pituitary, spinal cord and serum. The results indicated that AVP regulation of antinociception was limited to the brain nuclei.     

Arginine vasotocin delays extinction of a conditioned avoidance behavior in neonatal chicks

One minute after single-trial avoidance conditioning, young cockerels received intracerebroventricular or intraperitoneal injections of saline or arginine vasotocin (dose range: 0.004 to 16 μg/chick). Retroactive enhancement of the learned response was observed 24 hours post-training for some dose levels, but not for others. A 0.4 μg vasotocin dose also delayed extinction when injected 9 minutes after training. Behavioral similarities between avian and mammalian responses to vasotocin and other neuroactive peptides are discussed.     

In vitro potentiation of the activity of synthetic ovine corticotropin-releasing factor by arginine vasopressin

The ability of arginine vasopressin (AVP) to potentiate the actions of synthetic ovine corticotropin-releasing factor (CRF) was examined using anterior pituitary fragments. Marked potentiation of ACTH release was observed upon incubating the fragments with a combination of 2 nM AVP and 1 nM CRF. Potentiation of CRF-induced ACTH release was also observed when the fragments were incubated with a combination of 1 nM AVP and 0.5 nM CRF. These results suggest that AVP may play a role in the release of ACTH from the adenohypophysis.     

Investigating high-amplitude oscillations in rat tail skin blood flow during core heating and cooling

In a separate paper, we describe high-amplitude oscillations in human skin blood flow (Q˙_sk). Using an open-loop model in rats, we independently modulated and clamped hypothalamic and skin temperatures. Central heating reliably induced these high-amplitude oscillations in tail Q˙_sk, which occurred at 0.41±0.03 Hz spanning 758.1±25.7 ms, and were comprised of high-amplitude peaks (496.8±87.6 AU) arising from a stable baseline (114.1±27.6 AU). Central cooling significantly reduced Q˙_sk, but not the amplitude, the frequency, width or baseline of the oscillations. These observations indicate that such high-amplitude oscillations are not primarily mediated via central thermal state. Instead, we believe these oscillations to be turned on by an elevated skin temperature.     

Arginine vasopressin and a vasopressin antagonist peptide: Opposite effects on extinction of active avoidance in rats

Systemic injection of arginine vasopressin (AVP) (1 μ/rat) significantly prolonged extinction of a pole-jump, active avoidance response in rats; lateral ventricular injection of 1000-fold less AVP (1 ng/rat) produced similar results. A new AVP analogue, [1-deaminopenicillamine-2-(O-methyl)-tyrosine]arginine vasopressin (dPTyr-(Me)AVP), is known to antagonize behavioral and vascular effects of exogenous AVP at molar ratios of 5:1. At a dose of 100 μ/rat (subcutaneously) dPTyr-(Me)AVP produces, by itself, a behavioral effect opposite to that of exogenous AVP, namely a facilitation of extinction. Injections of dPTyr-(Me)AVP into the lateral ventricle were ineffective except at a dose of 10 μg/rat. These results confirm previous reports of the effect of vasopressin on delaying extinction of avoidance behavior, but suggest a site of action distant from the lateral ventricle.     

Arginine vasopressin 1a receptor gene and maternal behavior: evidence of association and moderation

This study examined associations among maternal sensitivity, mothers' early adversity and the Arginine Vasopressin 1a Receptor (AVPR1A) gene. Early adversity in mothers' background has been found to be associated with lower maternal sensitivity. Animal literature suggests that variation in the AVPR1A gene is associated with parenting quality. The goal of the study was to examine the role of the AVPR1A gene in maternal sensitivity, especially under conditions of high early adversity. Participants included 151 Caucasian women from a community sample. The women were videotaped in their home while interacting separately with two of their children (target child = 18 months, older sibling <6 years). Evidence was found for an association between the AVPR1A gene and maternal sensitivity. Mothers with two copies of the long RS3 alleles were less sensitive than mothers with one or zero copies of the long alleles. This association was strongest under conditions of high maternal early adversity.     

Morphological correlates of tail length in the catarrhine sacrum

Taillessness is a distinctive synapomorphy of the Hominoidea that has implications for interpretation of the locomotor behaviors and phylogenetic affinities of the clade’s earliest members. However, difficulties persist in confidently identifying taillessness in the catarrhine fossil record, stemming largely from our limited knowledge of the anatomical features with which the tail is associated. Here, we compare the morphology of the sacrum, the sole bony link between the tail and the rest of the body, among extant tailless hominoids and a broad sample of extant cercopithecoids known to vary in tail length (i.e., ‘very short’, ‘short’, and ‘long’) in order to identify morphological correlates of tail length. We examine three features of the sacrum, including the shape of the sacrum’s caudal articular surface (CAS), the sacrocaudal articulation (SCA) angle, and the lateral expansion of the last sacral vertebra’s transverse processes. Compared with all other taxa, ‘long’-tailed cercopithecoids have significantly more circularly-shaped CASs, more acute SCA angles, and more laterally expanded transverse processes of the last sacral vertebra. Tailless hominoids have significantly more elliptically-shaped CASs and less laterally expanded transverse processes than all tailed cercopithecoids, but in the latter parameter, they only differ significantly from ‘long’-tailed cercopithecoids. Cercopithecoids with ‘short’ and ‘very short’ tails are intermediate between tailless hominoids and ‘long’-tailed cercopithecoids with respect to CAS shape and lateral expansion of the transverse processes. SCA angle distinguishes clearly among all three cercopithecoid tail length groups. The results of this study provide evidence for significant differences in sacral morphology among extant catarrhines known to differ in tail length, and have implications for making inferences about tail length and function in extinct catarrhines.     

Intragranular co-storage of neuropeptide Y and arginine vasopressin in the paraventricular magnocellular neurons of the rat hypothalamus

Summary Certain populations of arginine vasopressin (AVP) neurons in the magnocellular paraventricular nucleus became immunoreactive for neuropeptide Y (NPY) when rats were treated with colchicine or monosodium glutamate (MSG). The co-storage of these peptides was examined by empooying a post-embedding electron-microscopic immunohistochemistry technique using goldlabeled antibodies to the two peptides. In colchicinetreated rats, the neuronal perikarya contained numerous secretory granules showing co-storage of the two peptides. The cells of the MSG-treated rats were characterized by having well-developed Golgi bodies with the granular structures also co-storing the two peptides, although the secretory granules in the perikarya were rather fewer than in the colchicine-treated rats. It is concluded that the destruction of the arcuate nucleus by MSG-treatment may potentiate the synthesis of NPY in AVP neurons, the synthesis of which is latent in intact animals.     

Sinoaortic denervation attenuates vasopressin-induced hypothermia and reduction of sympathetic nerve activity innervating brown adipose tissue in rats

It is well known that sympathetic nerve activity innervating brown adipose tissue (BAT sympathetic nerve activity) plays an important role in BAT thermogenesis. We have found that peripheral administration of arginine vasopressin (AVP) induced hypothermia by reduced thermogenesis in BAT. However, little is known about AVP-induced hypothermic response and its relationship with BAT sympathetic nerve activity. Because increases in baroreceptor inputs inhibit peripheral sympathetic nervous activity, we hypothesized that AVP-induced hypothermia is related to baroreceptor reflex suppression of BAT sympathetic nerve activity. To test this hypothesis, Male Sprague-Dawley rats were subjected to sinoaortic denervation or sham denervation, and implanted with radiotelemetry transmitters to assess the effects of peripheral administration of AVP on BAT sympathetic nerve activity, core and BAT temperatures. In sham-operated rats, an intraperitoneal (i.p.) injection of 10 µg/kg AVP led to a significant decrease in core and BAT temperatures. However, sinoaortic denervation significantly reduced the fall of core and BAT temperatures induced by AVP, compared with levels in sham-operated rats. AVP (10 µg/kg i.p.) rapidly decreased BAT sympathetic nerve activity in control and sham-operated rats, with the greatest levels of suppression occurring at 35 min and these lowest levels attained were with 30.6% and 29.24%, respectively. Furthermore, we found that sinoaortic denervation attenuated the suppressive effects of AVP (10 µg/kg i.p.) on BAT sympathetic nerve activity. The greatest level of suppression was only 20.8% occurring at 35 min after AVP. Therefore, these results indicate that the hypothermic effects of peripheral administration of AVP are partially mediated by the arterial baroreceptor reflex suppression of BAT sympathetic nerve activity and BAT thermogenesis.