ArticleBrain pathology (Zurich, Switzerland)2008
Adrenomedullin expression is up-regulated by acute hypobaric hypoxia in the cerebral cortex of the adult rat.
Article in Brain pathology (Zurich, Switzerland), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Temporal profiles of blood pressure, circulating nitric oxide, and adrenomedullin as predictors of clinical outcome in acute ischemic stroke patients.Molecular medicine reports · 2016Trial
- Adrenomedullin Is a Diagnostic and Prognostic Biomarker for Acute Intracerebral Hemorrhage.Current issues in molecular biology · 2021Article
- Lack of adrenomedullin in mouse endothelial cells results in defective angiogenesis, enhanced vascular permeability, less metastasis, and more brain damage.Scientific reports · 2016Article
- Short-term hypoxia/reoxygenation activates the angiogenic pathway in rat caudate putamen.Journal of biosciences · 2013Article
- Upregulation of transcription factor NRF2-mediated oxidative stress response pathway in rat brain under short-term chronic hypobaric hypoxia.Functional & integrative genomics · 2011Article
- High sensitivity to carcinogens in the brain of a mouse model of Alzheimer's disease.Oncogene · 2010Article
- Lack of adrenomedullin in the mouse brain results in behavioral changes, anxiety, and lower survival under stress conditions.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
Hypobaric hypoxia can produce neuropsychological disorders such as insomnia, dizziness, memory deficiencies, headache and nausea. Here we report the changes in adrenomedullin (AM) expression observed in rats exposed to hypobaric hypoxia and different times of reoxygenation. AM immunoreactivity was transiently elevated in the cerebral cortex after 7 h of exposure to a simulated altitude of 8325 m (27 000 ft). This higher expression was seen in all pyramidal cells and in a subset of small interneurons. AM-positive nonpyramidal neurons contained also calbindin and calretinin, but no parvalbumin immunoreactivity, thus identifying them as bipolar and double bouquet cells. Small blood vessels and related astroglia also became immunoreactive following the hypobaric insult. AM up-regulation decreased progressively with the time of reoxygenation, reaching almost control levels after 5 days. Real-time PCR quantification of AM mRNA and Western blotting confirmed the up-regulation of AM expression following hypobaria. In addition, hypobaria modulates alternative splicing of the AM gene resulting in a higher production of AM. Our data show that AM expression regulation constitutes a cortical response to hypobaria, suggesting that AM modulation may provide new therapeutic avenues to prevent and/or treat the symptoms produced by hypobaria.
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