Myelin/oligodendrocyte specific protein was compared to glial fibrilla
ry acidic protein and 2'3'-cyclic nucleotide 3'-phosphodiesterase expr
ession in normal rat brains and following stab wounds to the cerebral
cortex, corpus callosum and hippocampus. Animals with stab wounds were
allowed to recover for 5, 15, 28, 45 and 70 days post-operation befor
e fixation by perfusion. Sections were reacted with antibodies against
myelin/oligodendrocyte specific protein, glial fibrillary acidic prot
ein and 2'3'-cyclic nucleotide 3'-phosphodiesterase, and observed by l
ight and electron microscopy. Normal cerebral cortex had very few myel
in/oligodendrocyte specific protein-positive and 2'3'-cyclic nucleotid
e 3'-phosphodiesterase-positive cells, but some glial fibrillary acidi
c protein-positive cells. The myelinated fibres of the corpus callosum
were heavily stained for myelin/oligodendrocyte specific protein but
unstained by glial fibrillary acidic protein or 2'3'-cyclic nucleotide
3'-phosphodiesterase antibodies. Some immunopositive cells were prese
nt in the corpus callosum and hippocampus with all three antibodies. A
fter stab wound myelin/oligodendrocyte specific protein-positive react
ive cells had more and longer processes and stained more intensely tha
n equivalent cells in normal brain. These cells were distributed along
the wound track, including within the cerebral cortex. The numbers of
these cells increased until 28 days post-operation and then decreased
so that very few were found at 70 days post-operation except in the c
orpus callosum. Where demyelination occurred myelin/oligodendrocyte sp
ecific protein-staining was lost. Staining for 2' 3'-cyclic nucleotide
3'-phosphodiesterase revealed a similar pattern. Glial fibrillary aci
dic protein-positive reactive cells, which were also more robust than
the normal cells, were more widely distributed. They increased in numb
er throughout the time periods studied and gliosis was evident on the
contralateral side. The glial fibrillary acidic protein-positive astro
cytes were also different from the myelin/oligodendrocyte specific pro
tein-positive and 2'3'-cyclic nucleotide 3'-phosphodiesterase-positive
oligodendrocytes in terms of cell shape. With electron microscopy mye
lin/oligodendrocyte specific protein-positive cells showed features ty
pical of immature oligodendrocytes. We conclude that the injury caused
a numerical increase in oligodendrocytes and that myelin/oligodendroc
yte specific protein is a good marker for the oligodendroglial respons
e and demyelination in pathological conditions.