Hypothalamic tryptophan hydroxylase and the hypothalamic-pituitary-adrenocortical response to water deprivation and hydration in vasopressin-deficient and normal rats

Nk, Popova; Ks, Naumenko; Ln, Maslova; Tg, Amstislavskaya; Nn, Melidi; Vv, Bulygina; Ln, Ivanova

doi:10.1007/s00424-002-0806-0

Cited by 10 publications

(7 citation statements)

References 25 publications

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“…These results suggest that nNOS gene expression in the PVN neurons may be regulated depending on the osmotic condition of the body. Interestingly, the plasma corticosterone level changed in parallel with the PVN nNOS expression under different water conditions; i.e., it was increased by water deprivation, in accordance with previous reports (Kiss et al, 1994;Watts, 2000;Popova et al, 2002), and partially recovered by 1 hr of rehydration. However, the nNOS gene does not carry a glucocorticoid response element in its upstream promoter region (Jeong et al, 2000).…”

Section: Discussion Nnos Expression In the Pvn And Plasma Corticosteronesupporting

confidence: 89%

Water‐deprivation‐induced expression of neuronal nitric oxide synthase in the hypothalamic paraventricular nucleus of rat

Ryu

Lee

et al. 2007

J of Neuroscience Research

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This study was conducted to define the molecular mechanism by which dehydration induces expression of neuronal nitric oxide synthase (nNOS) in the hypothalamic paraventricular nucleus (PVN). Rats were deprived from water for 48 hr and then sacrificed immediately or 1 hr after ad libitum access to water. Another group of rats had free access to food and water and was included as euhydrate control group. The PVN sections fixed with 4% paraformaldehyde were processed for nNOS immunohistochemistry and NADPH-diaphorase (NADPH-d)/pCREB or NADPH-d/c-Fos double staining. nNOS-ir neurons significantly increased with water deprivation and decreased with rehydration, both in the posterior magnocellular (pM)- and the medial parvocellular (mP)-PVN. Most NADPH-d histostained neurons in the PVN appeared to exhibit pCREB-ir as well. Water deprivation markedly increased, and rehydration decreased, NADPH-d/pCREB neurons both in the pM- and in the mP-PVN. Gel shift assay demonstrated that dehydration may promote CREB binding to nNOS promoter in the PVN neurons. Significant amounts of NADPH-d-stained neurons in the PVN of water-deprived rats (67-68% in both the mP and the pM) exhibited c-Fos-ir. NADPH-d/c-Fos neurons in the pM-PVN were increased by water deprivation but not changed by rehydration. NADPH-d/c-Fos double-stained neurons in the mP-PVN did not significantly change depending on different water conditions. These results suggest that pCREB may play a role in dehydration-induced nNOS gene expression in the PVN neurons, and c-Fos might not be implicated in the regulatory pathway.

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Section: Discussion Nnos Expression In the Pvn And Plasma Corticosteronesupporting

confidence: 89%

Water‐deprivation‐induced expression of neuronal nitric oxide synthase in the hypothalamic paraventricular nucleus of rat

Ryu

Lee

et al. 2007

J of Neuroscience Research

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“…Our current results support our previous results by demonstrating that serotonin and AVP can interact to regulate the renal response to a natural osmotic challenge [32]. They also extend them by showing that serotonin is able to prevent the activity of the AVP system in the area of the anterior hypothalamus from being depressed by impulses from osmoreceptors under natural water intake.…”

Section: Discussionsupporting

confidence: 81%

“…Our previous studies in Wistar and AVP-deficient Brattleboro rats have demonstrated the involvement of the serotonin brain system in the central mechanisms of water balance regulation [32]. These results suggested that not only may serotonin participate in the regulation of AVP secretion, but AVP may also modulate serotonin metabolism and the response of the serotonergic system to water deprivation.…”

Section: Introductionmentioning

confidence: 83%

Effect of an Increase in Brain Serotonin on the Osmoregulatory Response to a Hypo- or Hyperosmotic Load in Wistar and Vasopressin-Deficient Brattleboro Rats

2007

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Serotonin and its receptor agonists stimulate the release of arginine vasopressin (AVP) into peripheral blood under intraventricular injection. To test the hypothesis that brain serotonin can modulate the development of natural osmoregulatory responses, the effect of an increase in endogenous brain serotonin on the response to an intragastric hypo- or hyperosmotic loading was studied in Wistar and AVP-deficient Brattleboro rats. 5-Hydroxytryptophan (5-HTP), the rate-limiting serotonin biosynthesis precursor known to increase the brain level of serotonin, was injected intraperitoneally (5 mg/100 g body weight). The renal functional parameters (glomerular filtration rate [GFR], free water reabsorption, and urine flow rate) were monitored during the 4 h after intragastric infusion of water or a 2% NaCl solution (5% of body weight). Plasma AVP was measured by radioimmunoassay. In Wistar rats, intraperitoneal injection of 5-HTP at the same time as water loading prevented the development of the renal diuretic response: there was no increase in urine flow rate and GFR, and free water reabsorption remained at the high level. In AVP-deficient Brattleboro rats, unlike Wistar rats, 5-HTP treatment was without effect on the renal function parameters. In Wistar rats, injection of 5-HTP at the peak of water diuresis produced an abrogation of the diuretic response to water loading due to the increase in free water reabsorption. Plasma AVP increased from 1.2 ± 0.4 to 4.2 ± 1.6 pg/ml (n = 8 in each group, p < 0.01). Hyperosmotic treatment of Wistar rats with a 2% NaCl solution stimulated AVP secretion compared to baseline (from 3.2 ± 0.1, n = 7 to 5.6 ± 0.9, n = 7, p < 0.01), and the saluretic response developed on the background of high free water reabsorption. When injected concomitantly with NaCl solution, 5-HTP revealed no additive effect on plasma AVP and on free water reabsorption. We conclude that the 5-HTP-caused increase in brain serotonin contributed significantly to the dynamics of changes in the osmoregulatory response to the hypo-osmotic challenge due to stimulation of AVP secretion. 5-HTP had no additive effect on the osmoregulatory response to hyperosmotic loading. Peripherally injected 5-HTP had no effect on the renal function, being absent in AVP-deficient Brattleboro rats.

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“…that AVP is required for the HPA response to osmotic stimuli. Water deprivation in Brattleboro rats led to a similar conclusion (Popova et al 2002). It is possible that oxytocin compensates for the loss of AVP in this process as it is also stimulated by osmotic challenges (Schlosser et al 1994).…”

Section: Discussionmentioning

confidence: 81%

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

Zelena

Domokos

Jain

et al. 2009

Journal of Endocrinology

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Adaptation to a constantly changing environment is fundamental to every living organism. The hypothalamicpituitary-adrenocortical (HPA) axis is a key component of the adaptation process. The present study tests the hypothesis that vasopressin (AVP) is required for the HPA response to acute stimuli. To accomplish this, naturally AVP-deficient Brattleboro rats were exposed to a wide range of stimuli and their HPA response was compared with heterozygous littermattes. The circadian rhythmicity of plasma ACTH and corticosterone was not different between the two genotypes. The ACTH and corticosterone response to volume load, restraint or aggressive attack were decreased in AVP-deficient rats. The stress-induced increase in ACTH, but not corticosterone, was significantly impaired in AVPdeficient animals after novelty, elevated plus-maze, forced swim, hypoglycaemia, ulcerogenic cold immobilisation, lipopolysaccharide, hypertonic saline and egg white injection. The HPA response to social avoidance, ether inhalation and footshock was not different between the genotypes. In vitro, the hypophysis of AVP-deficient animals showed a reduction in stimulated ACTH production and their adrenal glands were hyporeactive to ACTH. A dissociation between the ACTH and corticosterone response was observed in several experiments and could not be explained by an earlier ACTH peak or enhanced adrenal sensitivity, suggesting the existence of paraadenohypophyseal neuroendocrine regulators. Loss of AVP affected the HPA response to a wide variety of stressors. Interestingly, the contribution of AVP to the HPA response was not specific for, nor limited to, a known stressor category. Thus, there is a context-specific requirement for AVP in stress-induced activation of the HPA axis.

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Hypothalamic tryptophan hydroxylase and the hypothalamic-pituitary-adrenocortical response to water deprivation and hydration in vasopressin-deficient and normal rats

Cited by 10 publications

References 25 publications

Water‐deprivation‐induced expression of neuronal nitric oxide synthase in the hypothalamic paraventricular nucleus of rat

Water‐deprivation‐induced expression of neuronal nitric oxide synthase in the hypothalamic paraventricular nucleus of rat

Effect of an Increase in Brain Serotonin on the Osmoregulatory Response to a Hypo- or Hyperosmotic Load in Wistar and Vasopressin-Deficient Brattleboro Rats

The stimuli-specific role of vasopressin in the hypothalamus–pituitary–adrenal axis response to stress

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