Nitric Oxide and Carbon Monoxide Have a Stimulatory Role in the Hypothalamic-Pituitary-Adrenal Response to Physico-Emotional Stressors in Rats*

Kim, C. Kwon; Rivier, Catherine

doi:10.1210/endo.141.6.7500

Cited by 47 publications

(9 citation statements)

References 55 publications

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“…Colocalizations of nNOS with neuropeptides (e.g., CRH, oxytocin (Oxt) and orexin) were found in defined parts of the hypothalamus (Yamada et al, 1996; Nylen et al, 2001; Cheng et al, 2003), suggesting that NO could also interact with CRH/Ucn. Furthermore, different lines of investigation implied NO as an important component influencing corticotropin (ACTH) secretion in rats experiencing physical or emotional stress (Rivier and Shen, 1994; Turnbull et al, 1998; Kim and Rivier, 2000). Moreover, NO is thought to be involved in mechanisms controlling feeding behavior and body mass in rats (Morley and Flood, 1991; Squadrito et al, 1993; Calka et al, 1994; De Luca et al, 1995; Isse et al, 1999).…”

mentioning

confidence: 99%

Colocalization of urocortin and neuronal nitric oxide synthase in the hypothalamus and Edinger‐Westphal nucleus of the rat

Spina¹,

Langnaese²,

Orlando³

et al. 2004

J of Comparative Neurology

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Different lines of studies suggest that both the corticotropin-releasing hormone-related peptide Urocortin I (Ucn) and the neuromodulator nitric oxide (NO) are involved in the regulation of the complex mechanisms controlling feeding and anxiety-related behaviors. The aim of the present study was to investigate the possible interaction between Ucn and NO in the hypothalamic paraventricular nucleus (PVN), an area known to be involved in the modulation of these particular behaviors. Therefore, we mapped local mRNA and peptide/protein presence of both Ucn and the NO producing neuronal NO synthase (nNOS). This investigation was extended to include the hypothalamic supraoptic nucleus (SON) and the Edinger-Westphal nucleus area (EW), the latter being one of the major cellular Ucn-expressing sites. Furthermore, we compared the two predominantly used laboratory rat strains, Wistar and Sprague-Dawley. Ucn mRNA and immunoreactivity were detected in the SON and in the EW. A significant difference between Wistar and Sprague-Dawley rats was found in mRNA levels in the EW. nNOS was detected in all brain areas analyzed, showing a significantly lower immunoreactivity in the PVN and EW of Sprague-Dawley versus Wistar rats. Contrary to some previous reports, no Ucn mRNA and only a very low immunoreactivity were detectable in the PVN of either rat strain. Interestingly, double-labeling immunofluorescence revealed that in the SON approximately 75% of all cells immunoreactive for Ucn were colocalized with nNOS, whereas in the EW only approximately 2% of the Ucn neurons were found to contain nNOS. These findings suggest an interaction between Ucn and NO signaling within the SON, rather than the PVN, that may modulate the regulation of feeding, reproduction, and anxiety-related behaviors.

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confidence: 99%

Colocalization of urocortin and neuronal nitric oxide synthase in the hypothalamus and Edinger‐Westphal nucleus of the rat

Spina¹,

Langnaese²,

Orlando³

et al. 2004

J of Comparative Neurology

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“…We found that, indeed, sc L‐NAME decreased the ACTH response to 50 μg/kg LPS, but surprisingly the icv administration of this reagent only had a marginal effect. As a comparable dose of icv L‐NAME interfered with the ability of shocks to release ACTH, and as we previously showed that this treatment markedly reduced hypothalamic NOS activity,42 it is unlikely that the lack of effect of the arginine derivative in endotoxemic rats was due to a faulty protocol. In trying to explain these unexpected results, it may be relevant to note that VP antibodies did not alter the influence of sc injected L‐NAME in rats administered 50 μg/kg LPS.…”

Section: Discussionmentioning

confidence: 62%

“…In view of the ability of systemic L‐NAME to augment the ACTH response to VP,18 we reasoned that if icv injected L‐NAME could reach the pituitary, it would alter the ACTH response to this peptide. Our previous results had indicated that 50 μg L‐NAME significantly blocked hypothalamic, but not pituitary NOS activity, whereas 250 μg blocked both 42. These data had suggested that 250 μg reached the pituitary, and the present experiment therefore focused on the 50‐μg dose.…”

Section: Resultsmentioning

confidence: 76%

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Role of Nitric Oxide in Regulating the Rat Hypothalamic‐Pituitary‐Adrenal Axis Response to Endotoxemia

Rivier

2003

Annals of the New York Academy of Sciences

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This work examines the role of nitric oxide (NO) in the periphery (i.e., on the pituitary) and the brain (particularly on corticotropin-releasing factor [CRF] and vasopressin [VP] neurons in the paraventricular nucleus [PVN] of the hypothalamus) as a modulator of the ACTH response to lipopolysaccharide. We previously showed that NO restricted the pituitary response to VP while it facilitated the synthesis of PVN CRF and VP. In our experience, only relatively high doses of lipopolysaccharide (>50 microg/kg, injected intravenously [i.v.]) cause detectable increases in PVN neuronal activation. Our hypothesis, therefore, was that pituitary NO-VP interactions would predominate in rats injected with a low dose of lipopolysaccharide (0.5 microg/kg, i.v.) while the stimulatory influence of the gas on PVN neuronal activity would play an important role following i.v. injection of a large dose of lipopolysaccharide (50 microg/kg, i.v.). We observed that the ability of 0.5 microg/kg lipopolysaccharide to release ACTH was significantly enhanced by the subcutaneous (s.c.), but not the intracerebroventricular (i.c.v.) injection of L-NAME, an arginine derivative that blocks NO synthesis. The effect of s.c. L-NAME was reversed by immunoneutralization of endogenous VP, which indicated that in this model, the ability of lipopolysaccharide to release ACTH depended, at least in part, on the influence exerted by NO on the pituitary response to VP. In rats injected with the high lipopolysaccharide dose, the s.c. injection of L-NAME decreased plasma ACTH levels compared to those in rats pretreated with the vehicle. The effect of s.c. L-NAME was not significantly altered by VP antibodies. These results indicate that in this model, the primary influence of NO was exerted in the PVN and/or its afferents and that it did not depend on a peripheral, VP-mediated effect of the gas. On the one hand, these data are at odds with our finding that the i.c.v. injection of L-NAME only marginally altered the ACTH response to the large dose of lipopolysaccharide. As i.c.v. injected L-NAME should have primarily decreased hypothalamic, but not pituitary NOS, its only modest influence on ACTH release may have been due to a balance between stimulating and inhibiting effects of NO within the brain. As high doses of lipopolysaccharide increase brain levels of prostaglandin, monoamine, and proinflammatory cytokines, it will be important to investigate the influence exerted by NO on these secretagogues and on their interactions with PVN CRF and VP neurons, which may help us resolve the issues raised by our results. Collectively, these data support our hypothesis that the mechanisms mediating the ACTH response to a low lipopolysaccharide concentration involve the inhibitory VP-mediated influence of NO on pituitary activity. By contrast, the stimulatory effect of high doses of lipopolysaccharide on ACTH release depends, at least in part, on the ability of NO to upregulate PVN neuronal activity.

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“…SnPP was dissolved in dimethylsulphoxide/water (1 : 1), kept protected from light, and injected subcutaneously at 60 mg/kg (Kim and Rivier 2000) every 8 h starting at the time of infection. Control animals received a corresponding volume of vehicle only.…”

Section: Methodsmentioning

confidence: 99%

Induction of haem oxygenase‐1 causes cortical non‐haem iron increase in experimental pneumococcal meningitis: evidence that concomitant ferritin up‐regulation prevents iron‐induced oxidative damage

Ren

Leib

Ferriero

et al. 2006

Journal of Neurochemistry

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Desferrioxamine inhibits cortical necrosis in neonatal rats with experimental pneumococcal meningitis, suggesting that iron-induced oxidative damage might be responsible for neuronal damage. We therefore examined the spatial and temporal profile of changes in cortical iron and iron homeostatic proteins during pneumococcal meningitis. Infection was associated with a steady and global increase of non-haem iron in the cortex, particularly in neuronal cell bodies of layer II and V, and in capillary endothelial cells. The non-haem iron increase was associated with induction of haem oxygenase (HO)-1 in neurones, microglia and capillary endothelial cells, whereas HO-2 levels remained unchanged, suggesting that the non-haem iron increase might be the result of HO-1-mediated haem degradation. Indeed, treatment with the haem oxygenase inhibitor tin protoporphyrin (which completely blocked the accumulation of bilirubin detected in HO-1-positive cells) completely prevented the infection-associated non-haem iron increase. The same cells also displayed markedly increased ferritin staining, the increase of which occurred independently of HO activity. At the same time, no increase in DNA/RNA oxidation was observed in infected animals (as assessed by in situ detection of 8-hydroxy[deoxy]guanosine), strongly suggesting that ferritin up-regulation protected the brain from iron-induced oxidative damage. Thus, although pneumococcal meningitis leads to an increase of cortical non-haem iron, protective mechanisms up-regulated in parallel prevent iron-induced oxidative damage. Cortical damage does not appear to be a direct consequence of increased iron, therefore.

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Nitric Oxide and Carbon Monoxide Have a Stimulatory Role in the Hypothalamic-Pituitary-Adrenal Response to Physico-Emotional Stressors in Rats*

Cited by 47 publications

References 55 publications

Colocalization of urocortin and neuronal nitric oxide synthase in the hypothalamus and Edinger‐Westphal nucleus of the rat

Colocalization of urocortin and neuronal nitric oxide synthase in the hypothalamus and Edinger‐Westphal nucleus of the rat

Role of Nitric Oxide in Regulating the Rat Hypothalamic‐Pituitary‐Adrenal Axis Response to Endotoxemia

Induction of haem oxygenase‐1 causes cortical non‐haem iron increase in experimental pneumococcal meningitis: evidence that concomitant ferritin up‐regulation prevents iron‐induced oxidative damage

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