Premium
Loss of axonal contact causes down‐regulation of the PLP gene in oligodendrocytes: evidence from partial lesions of the optic nerve
Author(s) -
McPHILEMY K.,
GRIFFITHS I. R.,
MITCHELL L. S.,
KENNEDY P. G. E.
Publication year - 1991
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1991.tb00725.x
Subject(s) - astrocytosis , myelin , immunostaining , optic nerve , neurofilament , myelin basic protein , axon , biology , axoplasmic transport , pathology , neuroscience , anatomy , central nervous system , medicine , immunohistochemistry
We have examined the influence that axons may have on the expression of proteolipid protein (PLP), the major myelin protein of the CNS. Partial transections were made of the optic nerve of adult rats to produce approximately a 50% loss of axons. Twenty‐eight days after lesioning, sections of the distal nerves were immunostained for GFAP and neurofilament protein and hybridized for PLP mRNA. The area of astrocytosis, as defined by GFAP immunostaining, usually exceeded the extent of axonal loss. PLP mRNA expression in oligodendrocytes in the denervated area of the lesioned nerve was reduced compared to the innervated zones of the lesioned nerve and the contralateral intact nerve. This down‐regulation correlated with the axonal loss rather than the area of astrocytosis. The data support the contention that axons are necessary for oligodendrocytes to maintain full expression of their major myelin protein genes.