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

I. Hua Wei, Chih Chia Huang, Chi Yu Tseng, Hung Ming Chang, Hui Chin Tu, Mang Hung Tsai, Chen Yuan Wen, Jeng Yung Shieh

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Excessive production of nitric oxide (NO) might have detrimental effects on the hypoxia-related neuropathology. This study aimed to test if mild hypoxic preconditioning (MHPC) would attenuate the pathological changes in the brainstem motoneurons having a different functional component after peripheral nerve crush injury (PNCI). Prior to PNCI treatment, young adult rats were caged in the mild hypoxic altitude chamber with 79 Torr of the partial oxygen concentration (p O2) (i.e., 0.5 atm at 5500 m in height) for 4 weeks to adapt the environmental changes. After that, all the animals having successfully crushed both the hypoglossal and vagus nerves (left-side) were allowed to survive for 3, 7, 14, 30 and 60 successive days in normoxic condition. Nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry revealed that MHPC reduces NADPH-d/nNOS expression in the hypoglossal nucleus (HN) and the dorsal motor nucleus of the vagus (DMN) at different time points after PNCI. The morphological findings were further ascertained by Western blot analysis of nNOS and nitrite assay for NO production. Both the morphological and quantitative results peaked at 7 days in HN, whereas for those in DMN were progressively increased up to 60 days following PNCI. The staining intensity of NADPH-d/nNOS(+) neurons, expression of nNOS protein, NO production levels as well as the neuronal loss in HN and DMN of MHPC rats following PNCI were attenuated, especially for those having a longer survival period over 14 days. The MHPC treatment might induce minute amounts of NO to alter the state of milieu of the experimental animals to protect against the PNCI.

Original languageEnglish
Pages (from-to)123-132
Number of pages10
JournalJournal of Chemical Neuroanatomy
Volume35
Issue number1
DOIs
Publication statusPublished - Jan 2008
Externally publishedYes

Fingerprint

Nerve Crush
Peripheral Nerve Injuries
Nitric Oxide Synthase Type I
Motor Neurons
Adenine
Brain Stem
Phosphates
Wounds and Injuries
Nitric Oxide
Far-Western Blotting
Hypoglossal Nerve
Vagus Nerve
Nitrites
Crush Injuries
Young Adult
Immunohistochemistry
Staining and Labeling
Oxygen
Neurons
Therapeutics

Keywords

  • Dorsal motor nucleus of vagus
  • Hypoglossal nucleus
  • Nitric oxide
  • Peripheral nerve crush injury

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Mild hypoxic preconditioning attenuates injury-induced NADPH-d/nNOS expression in brainstem motor neurons of adult rats. / Wei, I. Hua; Huang, Chih Chia; Tseng, Chi Yu; Chang, Hung Ming; Tu, Hui Chin; Tsai, Mang Hung; Wen, Chen Yuan; Shieh, Jeng Yung.

In: Journal of Chemical Neuroanatomy, Vol. 35, No. 1, 01.2008, p. 123-132.

Research output: Contribution to journalArticle

Wei, I. Hua ; Huang, Chih Chia ; Tseng, Chi Yu ; Chang, Hung Ming ; Tu, Hui Chin ; Tsai, Mang Hung ; Wen, Chen Yuan ; Shieh, Jeng Yung. / Mild hypoxic preconditioning attenuates injury-induced NADPH-d/nNOS expression in brainstem motor neurons of adult rats. In: Journal of Chemical Neuroanatomy. 2008 ; Vol. 35, No. 1. pp. 123-132.
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AU - Huang, Chih Chia

AU - Tseng, Chi Yu

AU - Chang, Hung Ming

AU - Tu, Hui Chin

AU - Tsai, Mang Hung

AU - Wen, Chen Yuan

AU - Shieh, Jeng Yung

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AB - Excessive production of nitric oxide (NO) might have detrimental effects on the hypoxia-related neuropathology. This study aimed to test if mild hypoxic preconditioning (MHPC) would attenuate the pathological changes in the brainstem motoneurons having a different functional component after peripheral nerve crush injury (PNCI). Prior to PNCI treatment, young adult rats were caged in the mild hypoxic altitude chamber with 79 Torr of the partial oxygen concentration (p O2) (i.e., 0.5 atm at 5500 m in height) for 4 weeks to adapt the environmental changes. After that, all the animals having successfully crushed both the hypoglossal and vagus nerves (left-side) were allowed to survive for 3, 7, 14, 30 and 60 successive days in normoxic condition. Nicotinamine adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and neuronal nitric oxide synthase (nNOS) immunohistochemistry revealed that MHPC reduces NADPH-d/nNOS expression in the hypoglossal nucleus (HN) and the dorsal motor nucleus of the vagus (DMN) at different time points after PNCI. The morphological findings were further ascertained by Western blot analysis of nNOS and nitrite assay for NO production. Both the morphological and quantitative results peaked at 7 days in HN, whereas for those in DMN were progressively increased up to 60 days following PNCI. The staining intensity of NADPH-d/nNOS(+) neurons, expression of nNOS protein, NO production levels as well as the neuronal loss in HN and DMN of MHPC rats following PNCI were attenuated, especially for those having a longer survival period over 14 days. The MHPC treatment might induce minute amounts of NO to alter the state of milieu of the experimental animals to protect against the PNCI.

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