NO inhibition of the magnocellular neuroendocrine system in rats is independent of cGMP signaling pathway

Terrell, Mary Lee; Salas, Nilson A.; Bui, Vuong; Summy-Long, Joan Y.; Kadekaro, Massako

doi:10.1016/s0014-4886(03)00305-4

Cited by 21 publications

(17 citation statements)

References 58 publications

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“…Immunohistochemical and in situ hybridization studies have shown that the enzyme NOS (4-6) and its mRNA (7), citrulline (8), the co-product of NO synthesis, as well as NADPH-diaphorase activity (9), a histochemical marker of NOS, are expressed in forebrain and hindbrain osmoregulatory networks. These findings, as well as results from microdialysis studies (10), indicate that NO is produced at these sites, thus having a potential to modulate the activity of these structures, either directly or indirectly by ; inserted table) and their neural circuitry regulating body fluid homeostasis. The presence of NO synthase (NOS) (4-6) and its mRNA (7), citrulline (8), the co-product of NO synthesis, as well as NADPH-diaphorase activity (9), a histochemical marker of NOS, are expressed throughout the structures in the lamina terminalis, hypothalamo-neurohypophyseal system, as well as hindbrain.…”

Section: Introductionmentioning

confidence: 66%

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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Nitric oxide (NO), a free radical gas produced endogenously from the amino acid L-arginine by NO synthase (NOS), has important functions in modulating vasopressin and oxytocin secretion from the hypothalamo-neurohypophyseal system. NO production is stimulated during increased functional activity of magnocellular neurons, in parallel with plastic changes of the supraoptic nucleus (SON) and paraventricular nucleus. Electrophysiological data recorded from the SON of hypothalamic slices indicate that NO inhibits firing of phasic and non-phasic neurons, while L-NAME, an NOS inhibitor, increases their activity. Results from measurement of neurohypophyseal hormones are more variable. Overall, however, it appears that NO, tonically produced in the forebrain, inhibits vasopressin and oxytocin secretion during normovolemic, isosmotic conditions. During osmotic stimulation, dehydration, hypovolemia and hemorrhage, as well as high plasma levels of angiotensin II, NO inhibition of vasopressin neurons is removed, while that of oxytocin neurons is enhanced. This produces a preferential release of vasopressin over oxytocin important for correction of fluid imbalance. During late pregnancy and throughout lactation, fluid homeostasis is altered and expression of NOS in the SON is down-and up-regulated, respectively, in parallel with plastic changes of the magnocellular system. NO inhibition of magnocellular neurons involves GABA and prostaglandin synthesis and the signal-transduction mechanism is independent of the cGMP-pathway. Plasma hormone levels are unaffected by icv 1H-[1, 2, 4]oxadiazolo-[4,3-a]quinoxalin-1-one (a soluble guanylyl cyclase inhibitor) or 8-Br-cGMP administered to conscious rats. Moreover, cGMP does not increase in homogenates of the neural lobe and in microdialysates of the SON when NO synthesis is enhanced during osmotic stimulation. Among alternative signal-transduction pathways, nitrosylation of target proteins affecting activity of ion channels is considered.

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Section: Introductionmentioning

confidence: 66%

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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“…In fact, several reports support a role for this pathway underlying NO actions within the SON/VPN (Furuyama et al 1993;Aguila, 1994;Melis & Argiolas, 1995;Briski, 1999;Yang & Hatton, 1999;Li et al 2003a;Vacher et al 2003) (but see Ozaki et al 2000;Terrell et al 2003). Within this context, we attempted to identify NO-receptive neurones in the SON by visualizing cGMPir.…”

Section: Identification Of No Receptive Cgmp-producing Cellular Elemmentioning

confidence: 99%

Cellular sources, targets and actions of constitutive nitric oxide in the magnocellular neurosecretory system of the rat

Stern

Zhang

2005

The Journal of Physiology

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Nitric oxide (NO) is a key activity-dependent modulator of the magnocellular neurosecretory system (MNS) during conditions of high hormonal demand. In addition, recent studies support the presence of a functional consitutive NO tone. The aim of this study was to identify the cellular sources, targets, signalling mechanisms and functional relevance of constitutive NO production within the supraoptic nucleus (SON). Direct visualization of intracellular NO, along with neuronal nitric oxide synthase (nNOS) and cGMP immunohistochemisty, was used to study the cellular sources and targets of NO within the SON, respectively. Our results support the presence of a strong NO basal tone within the SON, and indicate that vasopressin (VP) neurones constitute the major neuronal source and target of basal NO. NO induced-fluorescence and cGMP immunoreactivity (cGMPir) were also found in the glia and microvasculature of the SON, suggesting that they contribute as sources/targets of NO within the SON. cGMPir was also found in association with glutamic acid decarboxylase 67 (GAD67)-and vesicular glutamate transporter 2 (VGLUT2)-positive terminals. Glutamate, acting on NMDA and possibly AMPA receptors, was found to be an important neurotransmitter driving basal NO production within the SON. Finally, electrophysiological recordings obtained from SON neurones in a slice preparation indicated that constitutive NO efficiently restrains ongoing firing activity of these neurones. Furthermore, phasically active (putative VP) and continuously firing neurones appeared to be influenced by NO originating from different sources. The potential roles for basal NO as an autocrine signalling molecule, and one that bridges neuronal-glial-vascular interactions within the MNS are discussed.

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“…In this regard, it was shown that NO plays an inhibitory role on the activity of MNCs, under physiological conditions (Liu et al, 1997), and that this modulation occurs by the activation of GABAergic synapses (Stern and Ludwig, 2001). However, other electrophysiological experiments have shown that this effect also occurs independently of GABAergic inputs and second messengers, suggesting that NO has a direct neuromodulatory effect on MNCs (Terrell et al, 2003;Ventura et al, 2008). Considering these facts, we aimed to analyze the role of NO on the electrical properties of magnocellular neurons subjected to a hypertonic solution.…”

Section: Introductionmentioning

confidence: 99%