| Literature DB >> 35771293 |
Shin Kikuchi1, Takayuki Kohno2, Takashi Kojima2, Haruyuki Tatsumi3, Yuki Ohsaki3, Takafumi Ninomiya3.
Abstract
Controlling axonal mitochondria is important for maintaining normal function of the neural network. Oxygen-glucose deprivation (OGD), a model used for mimicking ischemia, eventually induces neuronal cell death similar to axonal degeneration. Axonal mitochondria are disrupted during OGD-induced neural degeneration; however, the mechanism underlying mitochondrial dysfunction has not been completely understood. We focused on the dynamics of mitochondria in axons exposed to OGD; we observed that the number of motile mitochondria significantly reduced in 1 h following OGD exposure. In our observation, the decreased length of stationary mitochondria was affected by the following factors: first, the halt of motile mitochondria; second, the fission of longer stationary mitochondria; and third, a transformation from tubular to spherical shape in OGD-exposed axons. Motile mitochondria reduction preceded stationary mitochondria fragmentation in OGD exposure; these conditions induced the decrease of stationary mitochondria in three different ways. Our results suggest that mitochondrial morphological changes precede the axonal degeneration while ischemia-induced neurodegeneration.Entities:
Keywords: Axon; Fission; Mitochondria; Oxygen–glucose deprivation (OGD)
Year: 2022 PMID: 35771293 DOI: 10.1007/s10571-022-01247-y
Source DB: PubMed Journal: Cell Mol Neurobiol ISSN: 0272-4340 Impact factor: 4.231