Transection of dysmyelinated optic nerve axons in adult rats lacking myelin basic protein.
Injury to myelin or oligodendrocytes may manifest as dysmyelinating or demyelinating conditions of the CNS. Previous studies using dysmyelinated animal models (myelin basic protein mutants) suggest possible axonal dysfunction with complete loss of myelin. In this present study, we evaluated retinal ganglion cell survival after axotomy in MBP mutants to determine if prolonged dysmyelination of CNS axons exerted a detrimental effect on neuronal survival. We demonstrated that the survival of retinal ganglion cells with dysmyelinated axons is identical to retinal ganglion cells with myelinated axons after survival times up to 180 days. In myelin diseases where axon transection is a consistent consequence of demyelination resulting in progressive neurological deterioration, the absence of myelin does not accelerate neuronal death.
Phokeo
V
V
Department of Pathology and Molecular Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON Canada.
Ball
A K
AK
D000818:Animals; D001369:Axons / Q000502:physiology; D019771:Axotomy; D002470:Cell Survival; D007150:Immunohistochemistry; D009154:Mutation / Q000502:physiology*; D004676:Myelin Basic Protein / Q000235:genetics*; D009186:Myelin Sheath / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D012016:Reference Values; D012165:Retinal Ganglion Cells / Q000502:physiology*; D013997:Time Factors
D004676:Myelin Basic Protein