Developmental changes of nitric oxide synthase expression in the rat hypothalamoneurohypophyseal system

Yuan, Qiuju; Scott, David E.; So, Kwok-Fai; Wu, Wutian

doi:10.1002/ar.a.20271

Cited by 14 publications

(8 citation statements)

References 45 publications

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“…Nitric oxide is an important activity-dependent modulator of the magnocellular neuroendocrine response to physiological stimuli such as stress, dehydration and lactation (Ryu et al, 2007; Srisawat et al, 2000; Stern, 2004). Neurons of the PVN and SON show robust NOS expression (Stern and Zhang, 2005; Yuan et al, 2006), and the application of NO precursors or NO donors preferentially facilitates synaptic GABA release (Stern and Ludwig, 2001; Li et al, 2002; 2003), consistent with a close functional and anatomical coupling of NO and GABA in the SON (Stern and Zhang, 2005). Although there is recent evidence for NO facilitation of glutamate release in the SON in vivo (Gillard et al, 2007), NO regulation of synaptic activity in the hypothalamus is primarily implicated in the facilitation of GABA release to modulate neuronal excitability (Krukoff, 1999; Yang et al, 2007; Zhang and Patel, 1998).…”

Section: Discussionmentioning

confidence: 76%

Glucocorticoids Regulate Glutamate and GABA Synapse-Specific Retrograde Transmission via Divergent Nongenomic Signaling Pathways

Shi¹,

Maxson²,

Franco³

et al. 2009

J. Neurosci.

179

149

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Glucocorticoids exert an opposing rapid regulation of glutamate and GABA synaptic inputs to hypothalamic magnocellular neurons via the activation of postsynaptic membrane-associated receptors and the release of retrograde messengers. Glucocorticoids suppress synaptic glutamate release via the retrograde release of endocannabinoids and facilitate synaptic GABA release via an unknown retrograde messenger. Here, we show that the glucocorticoid facilitation of GABA inputs is due to the retrograde release of neuronal nitric oxide and that glucocorticoid-induced endocannabinoid synthesis and nitric oxide synthesis are mediated by divergent G-protein signaling mechanisms. While the glucocorticoid-induced, endocannabinoid-mediated suppression of glutamate release is dependent on activation of the G ␣ s G-protein subunit and cAMP-cAMP-dependent protein kinase activation, the nitric oxide facilitation of GABA release is mediated by G ␤ ␥ signaling that leads to activation of neuronal nitric oxide synthase. Our findings indicate, therefore, that glucocorticoids exert opposing rapid actions on glutamate and GABA release by activating divergent G-protein signaling pathways that trigger the synthesis of, and glutamate and GABA synapse-specific retrograde actions of, endocannabinoids and nitric oxide, respectively. The simultaneous rapid stimulation of nitric oxide and endocannabinoid synthesis by glucocorticoids has important implications for the impact of stress on the brain as well as on neural-immune interactions in the hypothalamus.

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Section: Discussionmentioning

confidence: 76%

Glucocorticoids Regulate Glutamate and GABA Synapse-Specific Retrograde Transmission via Divergent Nongenomic Signaling Pathways

Shi¹,

Maxson²,

Franco³

et al. 2009

J. Neurosci.

179

149

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“…NO also appears to play a role in development by regulating synapse formation and patterning (Hindley et al, 1997; Mogi et al, 2007; Scala et al, 2007; Vincent, 2010). Recent studies indicate that NO contributes to triggering a switch from cellular proliferation to differentiation during neurogenesis (Gibbs, 2003; Yuan et al, 2006; Vincent, 2010). Thus, the expression of nNOS in the mouse basolateral amygdalar complex (BLC) from embryonic Day 15.5 to adult has been studied (Olmos et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

The Expression of Neuronal Nitric Oxide Synthase in the Brain of the Mouse During Embryogenesis

Shao

Zhou

Rudd

et al. 2012

The Anatomical Record

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The distribution of neuronal nitric oxide synthase (nNOS) in the process of normal mouse brain growth from embryonic (E) Day 11 to postnatal (P) Day 1 was investigated by means of immunohistochemical and immunofluorescent methods. Our results demonstrated that nNOS positive neurons appeared early in superficial cortex at E11. At E13, nNOS positive neurons were located in lateral hypothalamus and amygdala, and temporarily in medullar and ventral hypothalamic neuroepithelia. From E15 to P0, nNOS positive neurons were distributed in superior and inferior colliculi, positive staining could also be seen in superior and inferior tectal neuroepithelium at E15. From E17 to birth, the medial geniculate nucleus had a high density of nNOS labeling. The distribution of nNOS gradually increased and extended laterally in embryo brain, which in turn implies that NO might be involved in the development of mouse brain. Anat Rec,

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“…Magnocellular region of PVN mainly contained vasopressin and oxytocin neurons as some paper reported (Arima and Aguilera 2000;Honda et al 2014). Nitric oxide synthase neurons were also located in the same region (Yuan et al 2006). These evidences implicated that the distribution of those neurons in the PVN were overlapped.…”

Section: Discussionmentioning

confidence: 76%

The interrelationship between cholinergic pathway in the magnocellular paraventricular nucleus and natriuresis

Wang

Wang²,

Zhang³

et al. 2015

gpb

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Abstract. The central nervous system is known to play important roles in the regulation of renal sodium excretion. The present study was designed to reveal the interrelationship between cholinergic pathway in the magnocellular paraventricular nucleus (PVN) and the natriuresis induced by brain cholinergic stimuli. The results indicated that urinary sodium excretion was significantly increased at 40 min after intracerebroventricular (ICV) injection of carbachol (CBC). Immunohistochemical studies showed that CBC increased choline acetyltransferase-immunoreactivity (ChAT-IR) in the magnocellular PVN and renal proximal convoluted tubule (PCT), respectively. After pretreatment with atropine, urinary sodium excretion was significantly reduced, and carbachol-increased ChAT-IR in the magnocellular PVN and PCT was also significantly decreased. These results suggested that brain cholinergic stimuli induced the natriuresis and increased the activity of cholinergic neurons in the magnocellular PVN and cholinergic system in the PCT. The blockade of muscarinic receptor completely abolished the natriuresis and partially inhibited carbachol-exerted stimulatory effects in the magnocellular PVN and PCT. To summarize, brain cholinergic pathway and peripheral cholinergic system in kidney were found to contribute to the natriuresis following brain cholinergic stimulation. Our findings revealed novel evidence that PVN was involved in the natriuresis via humoral mechanisms.

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Developmental changes of nitric oxide synthase expression in the rat hypothalamoneurohypophyseal system

Cited by 14 publications

References 45 publications

Glucocorticoids Regulate Glutamate and GABA Synapse-Specific Retrograde Transmission via Divergent Nongenomic Signaling Pathways

Glucocorticoids Regulate Glutamate and GABA Synapse-Specific Retrograde Transmission via Divergent Nongenomic Signaling Pathways

The Expression of Neuronal Nitric Oxide Synthase in the Brain of the Mouse During Embryogenesis

The interrelationship between cholinergic pathway in the magnocellular paraventricular nucleus and natriuresis

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