Reversible Disruption of Neuronal Mitochondria by Ischemic and Traumatic Injury Revealed by Quantitative Two-Photon Imaging in the Neocortex of Anesthetized Mice.
Mikhail KislinJeremy SwordIoulia V FomitchevaDeborah CroomEvgeny PryazhnikovEero LihavainenDmytro ToptunovHeikki RauvalaAndre S RibeiroLeonard KhirougSergei A KirovPublished in: The Journal of neuroscience : the official journal of the Society for Neuroscience (2017)
During ischemic stroke or brain trauma, mitochondria can either protect neurons by supplying ATP and adsorbing excessive Ca2+, or kill neurons by releasing proapoptotic factors. Mitochondrial function is tightly linked to their morphology: healthy mitochondria are thin and long; dysfunctional mitochondria are thick (swollen) and short (fragmented). To date, fragmentation of mitochondria was studied either in dissociated cultured neurons or in brain slices, but not in the intact living brain. Using real-time in vivo two-photon microscopy, we quantified mitochondrial fragmentation during acute pathological conditions that mimic severe, moderate, and mild brain injury. We demonstrated that alterations in neuronal mitochondria structural integrity can be reversible in traumatic and ischemic injuries, highlighting mitochondria as a potential target for therapeutic interventions.
Keyphrases
- cerebral ischemia
- brain injury
- cell death
- reactive oxygen species
- endoplasmic reticulum
- high resolution
- subarachnoid hemorrhage
- spinal cord
- spinal cord injury
- resting state
- white matter
- high throughput
- oxidative stress
- functional connectivity
- physical activity
- single molecule
- liver failure
- skeletal muscle
- drug induced
- ischemia reperfusion injury
- weight loss
- high intensity
- photodynamic therapy
- early onset
- single cell
- optical coherence tomography
- high fat diet induced
- hepatitis b virus
- protein kinase