Inhibition of nitric oxide synthase promotes facial axonal regeneration following neurorrhaphy

Wang, Shang-Ming; Tsai, Hui-Ping; Huang, Jiun-Jen; Huang, Hsuan-Chi; Lin, Jia-Li; Liu, Pei‐Hsin

doi:10.1016/j.expneurol.2009.01.006

Cited by 25 publications

(37 citation statements)

References 52 publications

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“…In addition, to verify the boundaries between cortical layers, selective sections were stained with cresyl violet or antiserum to protein gene product 9.5 (data not shown) as previously described (Wang et al, 2009). …”

Section: Cytochrome Oxidase Reactionmentioning

confidence: 99%

Ascorbic Acid Prevents Blood–Brain Barrier Disruption and Sensory Deficit Caused by Sustained Compression of Primary Somatosensory Cortex

Lin

Huang

Shen

et al. 2010

J Cereb Blood Flow Metab

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Transient compression of rat somatosensory cortex has been reported to affect cerebral microvasculature and sensory function simultaneously. However, the effects of long-term cortical compression remain unknown. Here, we investigated whether and to what extent sustained but moderate epidural compression of rat somatosensory cortex impairs somatic sensation and/or cortical microvasculature. Electrophysiological and behavioral tests revealed that sustained compression caused only short-term sensory deficit, particularly at 1 day after injury. Although the diameter of cortical microvessels was coincidentally reduced, no ischemic insult was observed. By measuring Evans Blue and immunoglobulin G extravasation, the blood-brain barrier (BBB) permeability was found to dramatically increase during 1 to 3 days, but this did not lead to brain edema. Furthermore, immunoblotting showed that the BBB component proteins occludin, claudin-5, type IV collagen, and glial fibrillary acidic protein were markedly upregulated in the injured cortex during 1 to 2 weeks when BBB regained integrity. Conversely, treatment of ascorbic acid prevented compression-induced BBB disruption and sensory impairment. Together, these data suggest that sustained compression of the somatosensory cortex compromises BBB integrity and somatic sensation only in the early period. Ascorbic acid may be used therapeutically to modulate cortical compression and/or BBB dysfunction.

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Section: Cytochrome Oxidase Reactionmentioning

confidence: 99%

Ascorbic Acid Prevents Blood–Brain Barrier Disruption and Sensory Deficit Caused by Sustained Compression of Primary Somatosensory Cortex

Lin

Huang

Shen

et al. 2010

J Cereb Blood Flow Metab

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“…nNOS or iNOS inhibition by the relatively specific inhibitors for nNOS 7-nitroindazole (7-NI), S-methyl-L-thiocitrulline (SMTC) and iNOS L-N6-(1-iminoethyl)-lysine hydrochloride (L-NIL), has contributed contradictory results. Whereas systemic administration of 7-NI, SMTC or L-NIL had beneficial effects on axonal regeneration after facial nerve transection and repair (Wang et al, 2009), positive effects were not obtained after XIIth nerve crushing by treatment with 7-NI or aminoguanidine (AG), another iNOS inhibitor (Sunico et al, 2008). Strikingly, administration of the relatively specific eNOS inhibitor L-N(5)-(l-iminoethyl)ornithine (L-NIO) accelerated the onset of muscle reinnervation after hypoglossal nerve crushing by promoting axonal regrowth (Sunico et al, 2008).…”

Section: Using An Avv To Accelerate and Improve Muscle Re-innervationmentioning

confidence: 92%

“…L-NAME also protected motoneurons from death and substantially increased the number that re-innervated the target muscle after facial nerve transection and repair, accompanied by improved motor function recovery (Wang et al, 2009). In the same direction, our studies showed that L-NAME treatment advanced the onset of neuromuscular reconnection after hypoglossal nerve crushing (Sunico et al, 2008).…”

Section: Using An Avv To Accelerate and Improve Muscle Re-innervationmentioning

confidence: 99%

Viral Vectors as Tools to Investigate the Role of Dysregulated Proteins in Nervous System Pathologies: the Case of Acquired Motor Neuropathies

Sunico¹,

Moreno‐López²

2011

Viral Gene Therapy

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“…nNOS, when confronted with peripheral nerve lesion, is known to induce a dramatic increase of NOS expression when affecting neuronal cell bodies. Therefore, NOS inhibition can promote improved axonal regeneration treatment of NOS inhibitors that can maintain the homeostasis of oxidative stress-related biomarkers, especially nNOS in neuronal cell bodies (Wang et al 2009). This offers a strong indication that production of NO by NOS can be dependent upon a variety of genetic factors and RNA regulations.…”

Section: The Regulatory Role Of No Isoforms In Cerebrovascular Tonementioning

confidence: 99%

Nitric Oxide as an Initiator of Brain Lesions During the Development of Alzheimer Disease

et al. 2009

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Nitric oxide (NO) is an important regulatory molecule for the host defense that plays a fundamental role in the cardiovascular, immune, and nervous systems. NO is synthesized through the conversion of L-arginine to L-citrulline by the enzyme NO synthase (NOS), which is found in three isoforms classified as neuronal (nNOS), inducible (iNOS), and endothelial (eNOS). Recent evidence supports the theory that this bioactive molecule has an influential role in the disruption of normal brain and vascular homeostasis, a condition known to elucidate chronic hypoperfusion which ultimately causes the development of brain lesions and the pathology that typify Alzheimer disease (AD). In addition, vascular NO activity appears to be a major contributor to this pathology before any overexpression of NOS isoforms is observed in the neuron, glia, and microglia of the brain tree, where the overexpression the NOS isoforms causes the formation of a large amount of NO. We hypothesize that since an imbalance between the NOS isoforms and endothelin-1 (ET-1), a human gene that encodes for blood vessel constriction, can cause antioxidant system insufficiency; by using pharmacological intervention with NO donors and/or NO suppressors, the brain lesions and the downstream progression of brain pathology and dementia in AD should be delayed or minimized.

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Inhibition of nitric oxide synthase promotes facial axonal regeneration following neurorrhaphy

Cited by 25 publications

References 52 publications

Ascorbic Acid Prevents Blood–Brain Barrier Disruption and Sensory Deficit Caused by Sustained Compression of Primary Somatosensory Cortex

Ascorbic Acid Prevents Blood–Brain Barrier Disruption and Sensory Deficit Caused by Sustained Compression of Primary Somatosensory Cortex

Viral Vectors as Tools to Investigate the Role of Dysregulated Proteins in Nervous System Pathologies: the Case of Acquired Motor Neuropathies

Nitric Oxide as an Initiator of Brain Lesions During the Development of Alzheimer Disease

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