Quantitative Analysis of Axonal Transport by Using Compartmentalized and Surface Micropatterned Culture of Neurons

Mitochondria, synaptic vesicles, and other cytoplasmic constituents have to travel long distance along the axons from cell bodies to nerve terminals. Interruption of this axonal transport may contribute to many neurodegenerative diseases including Alzheimer’s disease (AD). It has been recently shown...

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Published in:ACS chemical neuroscience 2012-06, Vol.3 (6), p.433-438
Main Authors: Kim, Hyung Joon, Park, Jeong Won, Byun, Jae Hwan, Poon, Wayne W, Cotman, Carl W, Fowlkes, Charless C, Jeon, Noo Li
Format: Article
Language:English
Subjects:
Alzheimer Disease - genetics
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Amyloid beta-Peptides - metabolism
Animals
Axonal Transport - physiology
Cell Compartmentation - physiology
Cells, Cultured
Humans
Image Processing, Computer-Assisted
Kymography - methods
Letter
Microfluidic Analytical Techniques - methods
Mitochondrial Membranes - metabolism
Mitochondrial Membranes - pathology
Neurons - metabolism
Neurons - pathology
Neurons - physiology
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Summary:Mitochondria, synaptic vesicles, and other cytoplasmic constituents have to travel long distance along the axons from cell bodies to nerve terminals. Interruption of this axonal transport may contribute to many neurodegenerative diseases including Alzheimer’s disease (AD). It has been recently shown that exposure of cultured neurons to β-amyloid (Aβ) resulted in severe impairment of mitochondrial transport. This Letter describes an integrated microfluidic platform that establishes surface patterned and compartmentalized culture of neurons for studying the effect of Aβ on mitochondria trafficking in full length of axons. We have successfully quantified the trafficking of fluorescently labeled mitochondria in distal and proximal axons using image processing. Selective treatment of Aβ in the somal or axonal compartments resulted in considerable decrease in mitochondria movement in a location dependent manner such that mitochondria trafficking slowed down more significantly proximal to the location of Aβ exposure. Furthermore, this result suggests a promising application of microfluidic technology for investigating the dysfunction of axonal transport related to neurodegenerative diseases.
ISSN:1948-7193
1948-7193
DOI:10.1021/cn3000026