Traumatic Brain Injury in the Rat Using the Fluid‐Percussion Model

Geoffrey S.F. Ling1, Eleanor Y. Lee1, Audrey N. Kalehua1

1 Uniformed Services University of the Health Sciences, Bethesda, Maryland
Publication Name:  Current Protocols in Neuroscience
Unit Number:  Unit 9.2
DOI:  10.1002/0471142301.ns0902s28
Online Posting Date:  September, 2004
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Traumatic brain injury is a leading cause of death and disability, particularly among young adults. During closed head trauma, the injury process is initiated by the impact of the brain against the inner table of the calvarium. Subsequently, there is prompt initiation of a complex biochemical, cellular, and physiological injury cascade that may take days to complete. From a functional standpoint, this culminates in neurologic dysfunction and, if severe, death. This unit describes an impact‐induced brain trauma model in rats which replicates nonpenetrating head injury. It does not model either penetrating or ischemic brain injuries.

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Table of Contents

  • Commentary
  • Literature Cited
  • Figures
  • Tables
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Basic Protocol 1:

  • Male Sprague‐Dawley rats (250 to 300 g)
  • Halothane
  • Oxygen
  • Surgical skin cleanser (e.g., Betadine)
  • Artificial Tears (The Butler Co.)
  • Cresyl violet dye (optional)
  • Gel foam
  • Cyanoacrylate glue
  • Saline: sterile 0.9% (w/v) NaCl
  • Bone wax
  • Fluid‐percussion device (Virginia Commonwealth University) consisting of:
    • 70‐cm pendulum fitted with a 4.8‐kg hammer head
    • 60‐cm‐long × 4.5‐cm‐diameter Plexiglas cylindrical fluid reservoir
    • Cork‐covered piston mounted on O rings bound to one end of the reservoir
    • Transducer mounted to the other end of the reservoir
    • 5‐cm‐long × 5‐mm‐diameter metal tube connected proximally to the transducer, with a male Luer‐Lok port at distal end
  • Oscilloscope with integrator (Tektronix or equivalent)
  • Strip chart recorder with pressure transducer (Gould Instrument Systems or equivalent)
  • 4‐way stopcock with Luer‐Lok fittings
  • Pressure tubing: 4‐foot (1.22‐m) clear pressure‐monitoring line with a male Luer‐Lok port at one end and a female Luer‐Lok port at the other end
  • Transducer calibration system (Spectramed or equivalent)
  • Carpenter's bubble level
  • Sharp knife
  • 27‐G, 0.5‐in. (1.27‐cm) sterile, disposable hypodermic needle
  • Fine file
  • Vaporizer
  • Vacuum trap for anesthetic vapors
  • Warming pad
  • Rectal temperature probe (Mallinckrodt Medical or equivalent)
  • Electric fur clippers
  • Scalpel and blade
  • Skin stapler and 9‐mm staples
  • Stereotaxic head frame for rats (ASI or equivalent)
  • Skin marker
  • Electric hand drill (Dremel or equivalent) with a 5‐mm trephine drill bit
  • Forceps, microdissecting
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Literature Cited

   Dietrich, W.D., Alonso, O., Busto, R., Globus, M.Y., and Ginsberg, M.D. 1994a. Post‐traumatic brain hypothermia reduces histopathological damage following concussive brain injury in the rat. Acta Neuropathol (Berl.) 87:250‐258.
   Dietrich, W.D., Alonso, O., and Halley, M. 1994b. Early microvascular and neuronal consequences of traumatic brain injury: A light and electron microscopic study in rats. J. Neurotrauma 11:289‐301.
   Dixon, C.E., Lyeth, B.G., Povlishock, J.T., Findling, R.L., Hamm, R.J., Marmarou, A., Young, H.F., and Hayes, R.L. 1987. A fluid percussion model of experimental brain injury in the rat. J. Neurosurg. 67:110‐119.
   Dixon, C.E., Lighthall, J.W., and Anderson, T.E. 1988. Physiologic, histopathologic, and cineradiographic characterization of a new fluid‐percussion model of experimental brain injury in the rat. J. Neurotrauma. 5:91‐104.
   Hayes, R.L., Jenkins, L.W., and Lyeth, B.G. 1991. Neurotransmitter‐mediated mechanisms of traumatic brain injury: Acetylcholine and excitatory amino acids. J. Neurotrauma. 9(Suppl 1):S173‐S187.
   Lighthall, J.W., Dixon, C.E., and Anderson, T.E. 1989. Experimental models of brain injury. J. Neurotrauma 6:83‐97.
   Long, J.B., Gordon, J., Bettencourt, J.A., and Bolt, S.L. 1996. Laser‐Doppler flowmetry measurements of subcortical blood flow changes after fluid percussion brain injury in rats. J. Neurotrauma 13:149‐162.
   Marion, D.W., Penrod, L.E., Kelsey, S.F., Obrist, W.D., Kochanek, P.M., Palmer, A.M., Wisniewski, S.R., and DeKosky, S.T. 1997. Treatment of traumatic brain injury with moderate hypothermia. New Engl. J. Med. 336:540‐546.
   McIntosh, T.K., Vink, R., Noble, L., Yamakami, I., Fernyak, S., Soares, H., and Faden, A.L. 1989. Traumatic brain injury in the rat: Characterization of a lateral fluid‐percussion model. Neuroscience 28:233‐244.
   Ommaya, A.K., Dannenberg, A.L., and Salazar, A.M. 1996. Causation, incidence, and costs of traumatic brain injury in the U.S. military medical system. J. Trauma 40:211‐217.
   Soares, H.D., Thomas, M., Cloherty, K., and McIntosh, T.K. 1992. Development of prolonged focal cerebral edema and regional cation changes following experimental brain injury in the rat. J. Neurochem. 58:1845‐1852.
   Toulmond, S., Duval, D., Serrano, A., Scatton, B., and Benavides, J. 1993. Biochemical and histological alterations induced by fluid percussion brain injury in the rat. Brain Res. 620:24‐31.
   Yamakami, I. and McIntosh, T.K. 1991. Alterations in regional cerebral blood flow following brain injury in the rat. J. Cereb. Blood Flow Metab. 11:655‐660.
   Zink, B.J. 1996. Traumatic brain injury. Emerg. Med. Clin. North Am. 14:115‐150.
Key References
   Dixon et al., 1987. See above.
  Description of the model.
   Lighthall et al., 1989. See above.
  Discusses advantages and disadvantages of the model.
   McIntosh et al., 1989. See above.
  Description of the model and neurologic changes.
   Toulmond et al., 1993. See above.
  Description of histopathologic changes after injury.
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