Citation

Olsson Y, Sharma HS, Pettersson A, Cervos-Navarro J. Prog. Brain Res. 1992; 91: 197-203.

Affiliation

Laboratory of Neuropathology, University Hospital, Uppsala, Sweden.

Copyright

(Copyright © 1992, Elsevier Publishing)

DOI

unavailable

PMID

1384082

Abstract

Trauma to the spinal cord induces a series of electrophysiological, immunological and biochemical events, but it is still unclear how such reactions are initiated and maintained. Most likely release of neurochemicals, breakdown of microvascular permeability and the formation of vasogenic edema play important roles in the pathophysiology of spinal cord trauma. In an animal model we have focused the attention to the possible involvement of endogenous serotonin, prostaglandins and opioid peptides in the formation of edema and associated disturbances of vascular permeability. The trauma was produced in anesthetized rats by making a focal lesion in the right dorsal horn at the T10-11 segments. This injury resulted in a profound increase in the microvascular permeability to 131I-sodium and an elevation of water content in the rostral T9 and caudal T12 segments as measured 5 h after the onset of the injury. Light microscopy of the perifocal changes in the T9-T12 segments using Nissl stain and immunohistochemistry to glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) showed profound cellular changes which were most severe in the ipsilateral ventral horn. Many nerve cell bodies were shrunken and the tissue had a spongy edematous appearance. There was a marked increase of GFAP immunoreactivity as well as a significant diminution of MBP staining. Pre-treatment with p-chlorophenylalanine (p-CPA, an endogenous serotonin depletor and synthesis inhibitor) or indomethacin (an endogenous prostaglandin synthesis inhibitor) or naloxone (an opioid receptor antagonist) significantly reduced the permeability changes and the edema formation.(ABSTRACT TRUNCATED AT 250 WORDS)

Language: en