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Hypoxia-induced expression of neuronal nitric oxide synthase in astrocytes of human corpus callosum

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Abstract

Nitric oxide (NO) is a gaseous neurotransmitter largely diffused in the brain; among other functions, it regulates the cerebral blood flow in response to hypoxia. NO can be synthetized by three different isoforms of the enzyme NO synthase: neuronal (nNOS), typical of neurons, endothelial and inducible. The aim of this study was to assess nNOS expression in human corpus callosum (CC) astrocytes, and its relationship with the hypoxia duration. Autoptic samples of CC from adult human subjects have been processed with immunohistochemistry and immunofluorescence using antibodies anti-nNOS and anti-glial fibrillary acidic protein (GFAP), the astrocyte marker. Results demonstrated for the first time the presence of nNOS-immunopositive astrocytes in the human CC. In particular, nNOS-positive astrocytes were absent in subjects deceased after a short hypoxia; their number and labeling intensity, however, increased with hypoxia prolongation. Neuronal NOS immunopositivity of CC astrocytes seems thus related to the hypoxia duration and the consequent brain damage.

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Funding

UNIVPM (PSA 2016) to M.F. Fellowship to T.L. was supported (60%) by PSA 2016.

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Correspondence to Mara Fabri.

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All procedures performed in the study were in accordance with the Ethics Committee of Università Politecnica delle Marche and conducted in accordance with the Helsinki Declaration of 1975, as revised in 2008.

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Lorenzi, T., Sagrati, A., Montanari, E. et al. Hypoxia-induced expression of neuronal nitric oxide synthase in astrocytes of human corpus callosum. Brain Struct Funct 226, 1353–1361 (2021). https://doi.org/10.1007/s00429-021-02244-5

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