Hypertonicity increases NO production to modulate the firing rate of magnocellular neurons of the supraoptic nucleus of rats

Silva, Melina P. da; Ventura, Raissa Wihby; Varanda, Wamberto Antônio

doi:10.1016/j.neuroscience.2013.06.067

Cited by 13 publications

(13 citation statements)

References 41 publications

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“…( b ) (48WD). As expected , we found an increase in the number of DAF2‐DA stained neurones, as well as an overall DAF2‐DA mean neuronal intensity in MNCs from 48WD compared to EU (both groups n = 6, P < 0.05 in both cases) (Fig. c,d ).…”

Section: Resultssupporting

confidence: 85%

Carbon Monoxide and Nitric Oxide interactions in Magnocellular Neurosecretory Neurones during Water Deprivation

Reis

Biancardi

Son

et al. 2015

J Neuroendocrinology

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Nitric oxide (NO) and carbon monoxide (CO) are diffusible gas messengers in the brain. Previously, we have shown their independent involvement in central fluid/electrolyte homeostasis control. In the present study, we investigated a possible functional interaction between NO/CO in the regulation of vasopressin (VP) and oxytocin (OT) magnocellular neurosecretory cells (MNCs) activity in euhydrated (EU) and dehydrated [48-h water-deprived (48WD)] rats. Using brain slices from EU and 48WD rats, we measured, by immunohistochemistry, the expression of neuronal NO synthase (nNOS, which synthesises NO) and haeme-oxygenase (HO-1, which synthesises CO) in the hypothalamic supraoptic nucleus (SON). In addition, we used patch-clamp electrophysiology to investigate whether regulation of SON MNC firing activity by endogenous CO was dependent on NO bioavailability and GABAergic inhibitory synaptic function. We found a proportion of OT and VP SON MNCs in EU rats to co-express both of HO-1 and nNOS (33.2 ± 2.9% and 15.3 ± 1.4%, respectively), which was increased in 48WD rats (55.5 ± 0.9% and 21.0 ± 1.7%, respectively, P < 0.05 for both). Inhibition of endogenous HO activity [chromium mesoporphyrin IX chloride (CrMP) 20 μm] induced MNC membrane hyperpolarisation and decreased firing activity, and these effects were blunted by previous blockade of endogenous NOS activity (l-NAME, 2 mm) or blockade of inhibitory GABA function [Picrotoxin (Sigma-Aldrich, St Louis, MO, USA), 50 μm]. No significant changes in SON NO bioavailability (4,5 diaminofluorescein diacetate fluorescence) were observed after CrMP treatment. Taken together, our results support a state-dependent functional inter-relationship between NO and CO in MNCs, in which CO acts as an excitatory gas molecule, whose effects are largely dependent on interactions with the inhibitory SON signals NO and GABA.

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Section: Resultssupporting

confidence: 85%

Carbon Monoxide and Nitric Oxide interactions in Magnocellular Neurosecretory Neurones during Water Deprivation

Reis

Biancardi

Son

et al. 2015

J Neuroendocrinology

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“…The inhibitory tonus provided by NO on the intrinsic excitability properties of MNs is also preserved in response to osmotic stress. Accordingly, it has been demonstrated that hypertonicity produces an increase in NOS expression and NO production, which is followed by a decrease in the firing frequency of MNs (26,110). Assuming that MNs function as osmoreceptors themselves and that hypertonicity is a potentially threatening condition that requires increased hormone secretion, it has been hypothesized that the hypertonicity-evoked NO inhibitory effect would exist as a protective mechanism through which reduced excitability would prevent overstimulation of MNs, thus avoiding saturation of the neurohypophyseal system (66).…”

Section: No: From An Endothelium-derived Relaxing Factor To a Neuromomentioning

confidence: 99%

“…Assuming that MNs function as osmoreceptors themselves and that hypertonicity is a potentially threatening condition that requires increased hormone secretion, it has been hypothesized that the hypertonicity-evoked NO inhibitory effect would exist as a protective mechanism through which reduced excitability would prevent overstimulation of MNs, thus avoiding saturation of the neurohypophyseal system (66). Based on the aforementioned findings, two main mechanisms underlie the inhibitory actions of NO: 1) stimulation of GABAergic inputs to MNs, consequently decreasing neuronal activity (98), and 2) changes in intrinsic neuronal properties, suggesting a direct action on ion channels (26,112). Regarding this latter effect, unpublished observations from our group suggest that NO may affect the activity of channels responsible for pacemaker generation in MNs, the so-called hyperpolarized activated cyclic nucleotide cation channels.…”

Section: No: From An Endothelium-derived Relaxing Factor To a Neuromomentioning

confidence: 99%

Gaseous Modulators in the Control of the Hypothalamic Neurohypophyseal System

et al. 2015

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Nitric oxide (NO), carbon monoxide (CO), and hydrogen sulfide (H2S) are gaseous molecules produced by the brain. Within the hypothalamus, gaseous molecules have been highlighted as autocrine and paracrine factors regulating endocrine function. Therefore, in the present review, we briefly discuss the main findings linking NO, CO, and H2S to the control of body fluid homeostasis at the hypothalamic level, with particular emphasis on the regulation of neurohypophyseal system output.

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“…Moreover, hyperosmotic stimulation induced NO production in MNCs in slices of the SON (52). This finding adds support to the hypothesis that osmotic stimulation induces an increase in NO production as a consequence of NOS overexpression (16,53).…”

Section: No Effects On the Mammalian Sonmentioning

confidence: 99%

Effects of nitric oxide on magnocellular neurons of the supraoptic nucleus involve multiple mechanisms

Silva

Cedraz-Mercez

Varanda

2014

Braz J Med Biol Res

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Physiological evidence indicates that the supraoptic nucleus (SON) is an important region for integrating information related to homeostasis of body fluids. Located bilaterally to the optic chiasm, this nucleus is composed of magnocellular neurosecretory cells (MNCs) responsible for the synthesis and release of vasopressin and oxytocin to the neurohypophysis. At the cellular level, the control of vasopressin and oxytocin release is directly linked to the firing frequency of MNCs. In general, we can say that the excitability of these cells can be controlled via two distinct mechanisms: 1) the intrinsic membrane properties of the MNCs themselves and 2) synaptic input from circumventricular organs that contain osmosensitive neurons. It has also been demonstrated that MNCs are sensitive to osmotic stimuli in the physiological range. Therefore, the study of their intrinsic membrane properties became imperative to explain the osmosensitivity of MNCs. In addition to this, the discovery that several neurotransmitters and neuropeptides can modulate their electrical activity greatly increased our knowledge about the role played by the MNCs in fluid homeostasis. In particular, nitric oxide (NO) may be an important player in fluid balance homeostasis, because it has been demonstrated that the enzyme responsible for its production has an increased activity following a hypertonic stimulation of the system. At the cellular level, NO has been shown to change the electrical excitability of MNCs. Therefore, in this review, we focus on some important points concerning nitrergic modulation of the neuroendocrine system, particularly the effects of NO on the SON.

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Hypertonicity increases NO production to modulate the firing rate of magnocellular neurons of the supraoptic nucleus of rats

Cited by 13 publications

References 41 publications

Carbon Monoxide and Nitric Oxide interactions in Magnocellular Neurosecretory Neurones during Water Deprivation

Carbon Monoxide and Nitric Oxide interactions in Magnocellular Neurosecretory Neurones during Water Deprivation

Gaseous Modulators in the Control of the Hypothalamic Neurohypophyseal System

Effects of nitric oxide on magnocellular neurons of the supraoptic nucleus involve multiple mechanisms

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