Axotomy along with Hypoxia Enhances the Neuronal NADPH-d/NOS Expression in Lower Brain Stem Motor Neurons of Adult Rats

Chang, Hong-Yeh; Lue, June‐Horng; Wen, Congcong; Shieh, Jeng-Yi

doi:10.1006/exnr.2001.7731

Cited by 18 publications

(30 citation statements)

References 38 publications

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“…At the peripheral level, nNOS accumulates in the growing motor axons, eNOS is overexpressed in vasa nervorum in the distal stump and around the injury site, and iNOS is also expressed by the recruited macrophages and phagocytic Schwann cells [33]. Upregulation of nNOS, but not iNOS [14], takes place at the soma of brainstem and spinal motoneurons, which are normally lacking in this enzyme, after peripheral compression, crush, transection, and avulsion injuries in various species [14, [136][137][138][139][140][141][142][143][144][145][146][147][148]. However, eNOS induction has not been reported in injured motoneurons.…”

Section: Nos Expression Timing and No Sources In Acquired Peripheral mentioning

confidence: 99%

“…Strikingly, in the rat, the percentage of nitrergic motoneurons relative to the total pool depended on type of lesion, with the higher percentages being observed after more severe lesions. Analysis of NADPH-diaphorase histochemistry to detect NOS expression revealed that a maximum of 24-27% of the total pool of motoneurons presented nitrergic attributes after nerve crushing [14, 140,147], while in more severe injuries the proportion increased: 48-60% after transection [140][141][142] and 80-98% after avulsion [136,138,140,148]. It is remarkable that in the rat the reduction in syn-ir density in motor nuclei after nerve crushing (−9% to −33%; [13, 14, 51]) was less extensive than after transection (−60% to −68%; [55, 60]) or avulsion (−70%; [67, 69]).…”

Section: Nos Expression Timing and No Sources In Acquired Peripheral mentioning

confidence: 99%

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NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

2010

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Synapse elimination is the main factor responsible for the cognitive decline accompanying many of the neuropathological conditions affecting humans. Synaptic stripping of motoneurons is also a common hallmark of several motor pathologies. Therefore, knowledge of the molecular basis underlying this plastic process is of central interest for the development of new therapeutic tools. Recent advances from our group highlight the role of nitric oxide (NO) as a key molecule triggering synapse loss in two models of motor pathologies. De novo expression of the neuronal isoform of NO synthase (nNOS) in motoneurons commonly occurs in response to the physical injury of a motor nerve and in the course of amyotrophic lateral sclerosis. In both conditions, this event precedes synaptic withdrawal from motoneurons. Strikingly, nNOS-synthesized NO is "necessary" and "sufficient" to induce synaptic detachment from motoneurons. The mechanism involves a paracrine/retrograde action of NO on pre-synaptic structures, initiating a downstream signaling cascade that includes sequential activation of (1) soluble guanylyl cyclase, (2) cyclic guanosine monophosphate-dependent protein kinase, and (3) RhoA/Rho kinase (ROCK) signaling. Finally, ROCK activation promotes phosphorylation of regulatory myosin light chain, which leads to myosin activation and actomyosin contraction. This latter event presumably contributes to the contractile force to produce ending axon retraction. Several findings support that this mechanism may operate in the most prevalent neurodegenerative diseases.

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Section: Nos Expression Timing and No Sources In Acquired Peripheral mentioning

confidence: 99%

Section: Nos Expression Timing and No Sources In Acquired Peripheral mentioning

confidence: 99%

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

2010

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“…Peroxynitrite is extremely reactive and has been implicated in lipid, protein and DNA damage [4]. Different experimental paradigms demonstrate that the rate of neuronal death closely paralleled the appearance of intense nNOS activity in neurons after axonal injury [5][6][7][8][9]. These results suggest that NO is related with neuronal death.…”

Section: Introductionmentioning

confidence: 87%

The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System

Yuan

Scott

et al. 2009

Neurochem Res

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Previous investigations from this laboratory have demonstrated that hypophysectomy induces up-regulation of neuronal nitric oxide synthase (nNOS) in magnocellular neurons of the mammalian hypothalamo-neurohypophyseal system (HNS). Accompanied by this upregulation of nNOS, both neuronal regeneration and degeneration are also observed in this system following hypophysectomy. The specific aim of this study was to determine the potential role of nNOS upregulation in neuronal survival and regeneration after hypophysectomy in the adult Sprague-Dawley (SD) rat by using a competitive nitric oxide synthase blocker, N(G)-nitrol-L: -arginine methyl ester (L: -NAME). We found that L: -NAME treatment effectively blocked the regeneration of magnocellular neurons of the rodent hypothalamus as observed in the lumen of the third cerebral ventricle following hypophysectomy. However, L: -NAME had no effect on the survival of magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei after hypophysectomy. These results suggest that the induced increase of nNOS expression enhance the regenerative ability of magnocellular neurons of the HNS following hypophysectomy.

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“…This up-regulation of enzyme is due to the excessive production of NO which might cause a detrimental effect on these neurons (Chang et al, 2001). Other studies using hippocampus brain slice of rats have shown that mild hypoxic episode-induced NO plays a key role to alter the state of the milieu by activation of nNOS via the release of appropriate amount of NO to protect against the subsequent severe hypoxic insult (Centeno et al, 1999;Perez-Pinzon and Born, 1999).…”

Section: Effects Of Nadph-d/nnos Expression In Mhpc/pnci Motoneuronsmentioning

confidence: 98%

“…Many serious diseases and pathologies might be due to under or over production of NO. Accumulating evidence have shown that peripheral nerve injury-induced expression of neuronal nitric oxide synthase (nNOS) as well as its mRNA seemed to signal the impending death of damaged cells, as the enzyme may act as a killer protein that produces neurotoxic levels of NO (Higuchi et al, 1996;Guo et al, 1997;Matsuoka et al, 1997;Bolanos and Almeida, 1999;Chang et al, 2000Chang et al, , 2001Chang et al, , 2002Chang et al, , 2003. Thus, to treat and to prevent the NO-related metabolic disorders become an important issue.…”

Section: Introductionmentioning

confidence: 98%

Mild hypoxic preconditioning attenuates injury-induced NADPH-d/nNOS expression in brainstem motor neurons of adult rats

Wei

Huang

Tseng³

et al. 2008

Journal of Chemical Neuroanatomy

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Axotomy along with Hypoxia Enhances the Neuronal NADPH-d/NOS Expression in Lower Brain Stem Motor Neurons of Adult Rats

Cited by 18 publications

References 38 publications

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

NO Orchestrates the Loss of Synaptic Boutons from Adult “Sick” Motoneurons: Modeling a Molecular Mechanism

The Potential Role of Nitric Oxide Synthase in Survival and Regeneration of Magnocellular Neurons of Hypothalamo-Neurohypophyseal System

Mild hypoxic preconditioning attenuates injury-induced NADPH-d/nNOS expression in brainstem motor neurons of adult rats

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