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- W2000306855 abstract "Abstract Cryolesion of the frontoparietal cortex in mice is a well‐described brain injury paradigm that results in increased astrogliosis surrounding the lesion site and is accompanied by a prominent increase in the MAO‐B levels in astrocytes. Whether these increased MAO‐B levels contribute to cellular damage or modulate reactive astrocytosis remains unclear. MAO‐B activity may contribute to cellular damage, since its metabolism products are highly toxic to the cells. Additionally, it has been suggested that MAO‐B inhibition may regulate astrocytic reaction. In this study, we have determined the relative contribution of MAO‐B activity to the outcome following freeze injury. Freeze injury induced a prominent increase of several inflammatory markers, including ICAM, Mac‐1, EB22, and GFAP. Inhibition of MAO‐B activity using the selective inhibitor PF9601N did not reduce this cryolesion‐induced inflammatory response. Additional data revealed that the expression of several cryolesion‐induced cell death genes, such as Fas, Rip, p53, and ICE, was not reduced in PF9601N‐treated mice, evidencing that MAO‐B activity did not contribute to cryolesion‐induced cell death. Definitive functional analysis of the mice using the ladder beam task revealed that MAO‐B inhibition did not improve the cryolesion‐induced motor impairment. These data strongly suggest that, although MAO‐B is highly expressed in the area surrounding the lesion site, its activity does not contribute to the cellular damage or play any role in regulating astrocytic reactivity. © 2008 Wiley‐Liss, Inc." @default.
- W2000306855 created "2016-06-24" @default.
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- W2000306855 date "2008-10-01" @default.
- W2000306855 modified "2023-10-10" @default.
- W2000306855 title "Monoamine oxidase-B activity is not involved in the neuroinflammatory response elicited by a focal freeze brain injury" @default.
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- W2000306855 doi "https://doi.org/10.1002/jnr.21892" @default.
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