Heatstroke-induced late-onset neurological deficits in mice caused by white matter demyelination, Purkinje cell degeneration, and synaptic impairment in the cerebellum

Global warming increases heatstroke incidence. After heatstroke, patients exhibit neurological symptoms, suggesting cerebellar damage. However, the potential long-term adverse outcomes are poorly understood. We studied the cerebellum after heatstroke in mouse heatstroke models. In this study, motor...

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Bibliographic Details
Published in:Scientific reports 2022-06, Vol.12 (1), p.10598-10598, Article 10598
Main Authors: Miyamoto, Kazuyuki, Nakamura, Motoyasu, Ohtaki, Hirokazu, Suzuki, Keisuke, Yamaga, Hiroki, Yanagisawa, Kaoru, Maeda, Atsuo, Yagi, Masaharu, Hayashi, Munetaka, Honda, Kazuho, Dohi, Kenji
Format: Article
Language:English
Subjects:
692/1807/1490
692/1807/2781
692/308/1426
692/420/256/2515
692/617/375/364
Animal models
Cell number
Cerebellum
Climate change
Corpus callosum
Degeneration
Demyelination
Global warming
Heatstroke
Humanities and Social Sciences
Motor ability
multidisciplinary
Myelin
Myelination
Neurological diseases
Postsynaptic density
Purkinje cells
Science
Science (multidisciplinary)
Substantia alba
Synaptophysin
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Summary:Global warming increases heatstroke incidence. After heatstroke, patients exhibit neurological symptoms, suggesting cerebellar damage. However, the potential long-term adverse outcomes are poorly understood. We studied the cerebellum after heatstroke in mouse heatstroke models. In this study, motor coordination disorder significantly appeared 3 weeks after heatstroke and gradually improved to some extent. Although white matter demyelination was detected at 1 and 3 weeks after heatstroke in the cerebellum, it was not found in the corpus callosum. The Purkinje cell numbers significantly decreased at 1, 3, and 9 weeks after heatstroke. The intensity of synaptophysin and postsynaptic density-95 temporarily appeared to attenuate at 3 weeks after heatstroke; however, both appeared to intensify at 9 weeks after heatstroke. Motor coordination loss occurred a few weeks after heatstroke and recovered to some extent. Late-onset motor impairment was suggested to be caused by cerebellar dysfunctions morphologically assessed by myelin staining of cerebellar white matter and immunostaining of Purkinje cells with pre- and postsynaptic markers. Purkinje cell number did not recover for 9 weeks; other factors, including motor coordination, partially recovered, probably by synaptic reconstruction, residual Purkinje cells, and other cerebellar white matter remyelination. These phenomena were associated with late-onset neurological deficits and recovery after heatstroke.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-022-14849-9