Conditional knockout of Mn superoxide dismutase in postnatal motor neurons reveals resistance to mitochondrial generated superoxide radicals

Hidemi Misawa, Kazuko Nakata, Junko Matsuura, Yasuhiro Moriwaki, Koichiro Kawashima, Takahiko Shimizu, Takuji Shirasawa, Ryosuke Takahashi

研究成果: Article査読

42 被引用数 (Scopus)

抄録

Mitochondrial dysfunction and oxidative damage are implicated in the pathogenesis of neurodegenerative disease. Mice deficient in the mitochondrial form of superoxide dismutase (SOD2) die during embryonic or early postnatal development, precluding analysis of a pathological role for superoxide in adult tissue. Here, we generated postnatal motor neuron-specific SOD2 knockouts by crossing mice with floxed SOD2 alleles to VAChT-Cre transgenic mice in which Cre expression is restricted to postnatal somatomotor neurons. SOD2 immunoreactivity was specifically lost in a subset of somatomotor neurons resulting in enhanced superoxide production. Yet extensive histological examination revealed no signs of oxidative damage in animals up to 1 year after birth. However, disorganization of distal nerve axons following injury was accelerated in SOD2-deficient motor neurons. These data demonstrate that postnatal motor neurons are surprisingly resistant to oxidative damage from mitochondrial-derived superoxide radicals, but that such damage may sensitize axons to disorganization following nerve injury.

本文言語English
ページ(範囲)169-177
ページ数9
ジャーナルNeurobiology of Disease
23
1
DOI
出版ステータスPublished - 2006 7月

ASJC Scopus subject areas

  • 神経学

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