Purkinje cell vulnerability to mild traumatic brain injury

Kazumasa Fukuda, Naoto Aihara, Stephan M. Sagar, Frank R Sharp, Lawrence H. Pitts, Jari Honkaniemi, L. J. Noble

Research output: Contribution to journalArticle

63 Citations (Scopus)

Abstract

In this study we examined the cerebellar response to mild traumatic brain injury by assessing microglial activation and Purkinje cell loss. Activated microglia were identified using the antibodies OX-42 and ED-1 as well as isolectin B4. The anti-Purkinje cell antibody PEP-19 was used to evaluate Purkinje cell loss after injury. The mechanism of cell injury was examined using a monoclonal antibody to the inducible 72-kDa heat shock protein. A monoclonal antibody to the N-terminal sequence of Fos was used as a marker for neuronal activation. There was progressive activation of microglia in the cerebellar vermis within a few days after forebrain injury. In coronal sections the processes of activated microglia were oriented in 'stripes' perpendicular to the cortical surface. In sagittal sections the activated microglia were in irregularly shaped clusters or in a fan-like distribution that radiated from the Purkinje cell layer toward the cortical surface. There was a significant loss of Purkinje cells 7 days postinjury as compared to the control group. There was no evidence of induction of heat shock protein in the cerebellum. In addition, there was no evidence of induction of c-Fos protein in either the cerebellar cortex or inferior olivary nuclei within the first 3 h after injury. These studies demonstrate that a fluid percussive impact to the forebrain results in cerebellar damage. The close anatomical association between activated microglia and Purkinje cells suggests that Purkinje cell injury is the cause of the microglial activation. The mechanism of Purkinje cell death, however, remains unclear.

Original languageEnglish (US)
Pages (from-to)255-266
Number of pages12
JournalJournal of Neurotrauma
Volume13
Issue number5
StatePublished - May 1996
Externally publishedYes

Fingerprint

Brain Concussion
Purkinje Cells
Microglia
Wounds and Injuries
Prosencephalon
Monoclonal Antibodies
HSP72 Heat-Shock Proteins
Olivary Nucleus
Proto-Oncogene Proteins c-fos
Cerebellar Cortex
Antibodies
Heat-Shock Proteins
Lectins
Cerebellum
Cell Death
Control Groups

Keywords

  • microglia
  • OX-42
  • PEP-19
  • Purkinje cell
  • traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Fukuda, K., Aihara, N., Sagar, S. M., Sharp, F. R., Pitts, L. H., Honkaniemi, J., & Noble, L. J. (1996). Purkinje cell vulnerability to mild traumatic brain injury. Journal of Neurotrauma, 13(5), 255-266.

Purkinje cell vulnerability to mild traumatic brain injury. / Fukuda, Kazumasa; Aihara, Naoto; Sagar, Stephan M.; Sharp, Frank R; Pitts, Lawrence H.; Honkaniemi, Jari; Noble, L. J.

In: Journal of Neurotrauma, Vol. 13, No. 5, 05.1996, p. 255-266.

Research output: Contribution to journalArticle

Fukuda, K, Aihara, N, Sagar, SM, Sharp, FR, Pitts, LH, Honkaniemi, J & Noble, LJ 1996, 'Purkinje cell vulnerability to mild traumatic brain injury', Journal of Neurotrauma, vol. 13, no. 5, pp. 255-266.
Fukuda K, Aihara N, Sagar SM, Sharp FR, Pitts LH, Honkaniemi J et al. Purkinje cell vulnerability to mild traumatic brain injury. Journal of Neurotrauma. 1996 May;13(5):255-266.
Fukuda, Kazumasa ; Aihara, Naoto ; Sagar, Stephan M. ; Sharp, Frank R ; Pitts, Lawrence H. ; Honkaniemi, Jari ; Noble, L. J. / Purkinje cell vulnerability to mild traumatic brain injury. In: Journal of Neurotrauma. 1996 ; Vol. 13, No. 5. pp. 255-266.
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