Neurotoxicity Research

, 13:71

Posttraumatic administration of pituitary adenylate cyclase activating polypeptide in central fluid percussion injury in rats

Authors

  • Erzsébet Kóvesdi
    • Department of NeurosurgeryUniversity of Pécs, Medical Faculty
  • Andrea Tamás
    • Department of AnatomyUniversity of Pécs, Medical Faculty
  • Dóra Reglodi
    • Department of AnatomyUniversity of Pécs, Medical Faculty
  • Orsolya Farkas
    • Department of RadiologyUniversity of Pécs, Medical Faculty
  • József PáL
    • Department of NeurosurgeryUniversity of Pécs, Medical Faculty
  • Gábor Tóth
    • Department of Medical ChemistryUniversity of Szeged
  • Péter Bukovics
    • Department of NeurosurgeryUniversity of Pécs, Medical Faculty
    • Clinical Neuroscience Research GroupHungarian Academy of Sciences
  • Tamás Dóczi
    • Department of NeurosurgeryUniversity of Pécs, Medical Faculty
    • Department of NeurosurgeryUniversity of Pécs, Medical Faculty
Article

DOI: 10.1007/BF03033558

Cite this article as:
Kóvesdi, E., Tamás, A., Reglodi, D. et al. neurotox res (2008) 13: 71. doi:10.1007/BF03033558

Abstract

Severalin vitro andin vivo experiments have demonstrated the neuroprotective effects of pituitary adenylate cyclase activating polypeptide (PACAP) in focal cerebral ischemia, Parkinson’s disease and traumatic brain injury (TBI). The aim of the present study was to analyze the effect of PACAP administration on diffuse axonal injury (DAI), an important contributor to morbidity and mortality associated with TBI, in a central fluid percussion (CFP) model of TBI. Rats were subjected to moderate (2 Atm) CFP injury. Thirty min after injury, 100 μg PACAP was administered intracerebroventricularly. DAI was assessed by immunohistochemical detection of β-amyloid precursor protein, indicating impaired axoplasmic transport, and RMO-14 antibody, representing foci of cytoskeletal alterations (neurofilament compaction), both considered classical markers of axonal damage. Analysis of damaged, immunoreactive axonal profiles revealed significant axonal protection in the PACAP-treated versus vehicletreated animals in the corticospinal tract, as far as traumatically induced disturbance of axoplasmic transport and cytoskeletal alteration were considered. Similarly to our former observations in an impact acceleration model of diffuse TBI, the present study demonstrated that PACAP also inhibits DAI in the CFP injury model. The finding indicates that PACAP and derivates can be considered potential candidates for further experimental studies, or purportedly for clinical trials in the therapy of TBI.

Keywords

Traumatic brain injury PACAP Axonoprotection APP RMO

Abbreviations

APP

Amyloid precursor protein

CFP

Central fluid percussion

CSpT

Corticospinal tract

DAI

Diffuse axonal injury; icv, intracerebroventricularly

MLF

Medial longitudinal fascicle

PACAP

Pituitary adenylate cyclase activating polypeptide

TBI

Traumatic brain injury

Copyright information

© Springer 2008