Advertisement

Microfluidic Device for Studying Traumatic Brain Injury

  • Yiing Chiing Yap
  • Tracey C. Dickson
  • Anna E. King
  • Michael C. Breadmore
  • Rosanne M. Guijt
Protocol
Part of the Neuromethods book series (NM, volume 126)

Abstract

Throughout the world, traumatic brain injury (TBI), for example, as a result of motor vehicle accident, is a major cause of mortality and lifelong disability in children and young adults. Studies show that axonal pathology and degeneration can cause significant functional impairment and can precede, and sometimes cause, neuronal death in several neurological disorders including TBI, creating a compelling need to understand the mechanisms of axon degeneration. Microfluidic devices that allow manipulation of fluids in channels with typical dimensions of tens to hundreds of micrometers have emerged as a powerful platform for such studies due to their ability to isolate and direct the growth of axons. Here, we describe a new microfluidic platform that can be used to study TBI by applying very mild (0.5%) and mild (5%) stretch injury to individual cortical axons through the incorporation of microfluidic valve technology into a compartmented microfluidic-culturing device. This device is unique due to its ability to study the neuronal response to axonal stretch injury in a fluidically isolated microenvironment.

Key words

Microfluidic Stretch injury Traumatic brain injury Quake valve Primary cell culture 

References

  1. 1.
    Sosin DM, Sniezek JE, Waxweller RJ (1995) Trends in death associated with traumatic brain injury, 1979 through 1992-sucess and failure. JAMA 273:1778–1780CrossRefPubMedGoogle Scholar
  2. 2.
    Povlishock JT (1992) Traumatically induced axonal injury-pathogenesis and pathobiological implications. Brain Pathol 2:1–12PubMedGoogle Scholar
  3. 3.
    Adams JH, Doyle D, Graham DI et al (1984) Diffuse axonal injury in head injuries caused by fall. Lancet 2:1420–1422CrossRefPubMedGoogle Scholar
  4. 4.
    Grady MS, McLaughlin MR, Christman CW et al (1993) The use of antibodies targeted against the neurofilament subunits for detection of diffuse injury in humans. J Neuropathol Exp Neurol 52:143–152CrossRefPubMedGoogle Scholar
  5. 5.
    Meaney DF, Smith DH, Shreiber DI et al (1995) Biochemical analysis of experimental diffuse axonal injury. J Neurotrauma 12:689–694CrossRefPubMedGoogle Scholar
  6. 6.
    Povlishock JT, Erb DE, Astruc J (1992) Axonal response to traumatic brain injury- reactive axonal change, differentiation and neuroplasticity. J Neurotrauma 9:S189–S200CrossRefPubMedGoogle Scholar
  7. 7.
    Coleman MP, Perry VH (2002) Axon pathology in neurological disease: a neglected therapeutic target. Trends Neurosci 25:532–537CrossRefPubMedGoogle Scholar
  8. 8.
    Raff MC, Whitmore AV, Finn JT (2002) Neuroscience - axonal self-destruction and neurodegeneration. Science 296:868–871CrossRefPubMedGoogle Scholar
  9. 9.
    Yap YC, Dickson TC, King AE, Breadmore MC, Guijt RM (2014) Microfluidic culture platform for studying neuronal response to mild to very mild axonal stretch injury. Biomicrofluidics 8:044110CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    Taylor AM et al (2005) A microfluidic culture platform for CNS axonal injury, regeneration and transport. Nat Methods 2:599–605CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer Science+Business Media LLC 2017

Authors and Affiliations

  • Yiing Chiing Yap
    • 1
    • 2
    • 3
    • 4
  • Tracey C. Dickson
    • 1
  • Anna E. King
    • 2
  • Michael C. Breadmore
    • 3
  • Rosanne M. Guijt
    • 4
  1. 1.Menzies Institute for Medical Research, University of TasmaniaHobartAustralia
  2. 2.Wicking Dementia Research and Education Centre, School of Medicine, University of TasmaniaHobartAustralia
  3. 3.Australian Centre for Research on Separation Science (ACROSS), School of Physical Sciences, University of TasmaniaHobartAustralia
  4. 4.School of Medicine and ACROSS, University of TasmaniaHobartAustralia

Personalised recommendations