myelin-basic-protein and Retinal-Diseases

This study evaluated the function of mouse optic nerves after transient retinal ischemia using in vitro electrophysiologic recordings of compound action potentials (CAPs) correlated with diffusion tensor imaging (DTI) injury markers with confirmation by immunohistochemistry-determined pathology.. Retinal ischemia was induced in 7- to 8-week-old female C57BL/6 mice by elevating intraocular pressure to 110 mm Hg for 60 minutes. At 3 and 7 days after retinal ischemia, optic nerves were removed for CAP measurements. The CAP amplitude was recorded using suction electrodes in isolated control and injured optic nerves followed by ex vivo DTI evaluation. After DTI, optic nerves were embedded in paraffin and cut for immunohistochemical analyses.. Consistent with previous in vivo DTI measurements, a 25% decrease in axial diffusivity with normal radial diffusivity was seen at 3 days after retinal ischemia, suggesting axonal injury without myelin damage. At 7 days, there was no additional change in axial diffusivity compared with that at 3 days, but radial diffusivity significantly increased by 50%, suggestive of significant myelin damage due to sustained axonal injury. The relative anisotropy (RA) progressively decreased after retinal ischemia when compared with that of the controls. The CAP amplitude in injured nerves also progressively decreased after retinal ischemia, which correlated with the reduced RA (r = 0.80).. This study suggests that CAP amplitude reflects both axonal and myelin integrity and RA is an optimal parameter for functional assessment compared with axial or radial diffusivity alone in murine optic nerves after retinal ischemia.

Topics: Action Potentials; Animals; Axons; Diffusion Tensor Imaging; Disease Models, Animal; Electrophysiology; Female; Mice; Mice, Inbred C57BL; Myelin Basic Protein; Myelin Sheath; Nerve Degeneration; Optic Nerve Diseases; Reperfusion Injury; Retinal Diseases; Retinal Ganglion Cells

The aim of this study was to characterize the serum antibody reactivities occurring after ocular ischemia reperfusion. The time course of serum antibody responses was examined.. Wistar rats were exposed to transient ocular ischemia by elevating intraocular pressure to 130 mm Hg for 60 minutes. Axonal damage was evaluated on optic-nerve sections 2 and 4 weeks later. Blood samples collected before and several times after ischemia were used for antibody detection via customized protein microarrays. Different tissue antigens, including heat shock proteins (HSPs) and crystallins, were selected based on previous identification of antibody reactivities in studies on ischemic events or ophthalmic diseases associated with ischemia. Antibody reactivity was compared using multivariate statistical techniques.. Significant axonal damage was observed 2 and 4 weeks after ocular ischemia (P < 0.05). Animals showed certain immunoreactivities against antigens even before ischemia, whereas many reactivities increased afterward. Significantly different responses were detected 2, 3, and 4 weeks after ischemia (P < 0.05). Antibody reactivity against actin, glial fibrillary acidic protein, HSP 27, vimentin, or spectrin continually increased.. Ischemia induced by acute intraocular pressure elevation led to complex changes in antibody reactivities in sera of treated animals. Upregulation of serum autoantibodies, especially against heat shock and structural proteins, progressively increased throughout the 4-week follow-up period, whereas others such as ubiquitin decreased. The upregulation of anti-HSP 27 antibodies might be an attempt to protect the tissue from ischemic damage.

Topics: Animals; Autoantibodies; Autoantigens; Axons; Eye Proteins; Glial Fibrillary Acidic Protein; HSP27 Heat-Shock Proteins; Immunoglobulin G; Intraocular Pressure; Male; Myelin Basic Protein; Myelin Proteins; Myelin-Associated Glycoprotein; Myelin-Oligodendrocyte Glycoprotein; Optic Nerve; Protein Array Analysis; Rats; Rats, Wistar; Reperfusion Injury; Retinal Diseases; Retinal Vessels; Spectrin; Up-Regulation

To further characterize the nature of retinal periphlebitis and retinitis in multiple sclerosis, immunoperoxidase studies were performed on retinal tissue from multiple sclerosis patients at autopsy. Antibodies against myelin basic protein stained the optic nerve but not the retina. Both normal and multiple sclerosis retinas showed staining of Müller cells with Leu-7 (a monoclonal antibody that cross-reacts with myelin associated glycoprotein and natural killer cells). Nerve fiber bundles of the optic nerve in cases with multiple sclerosis and controls also showed staining with Leu-7 antibody. Tissue-bound IgG was demonstrated on retinal ganglion cells in six of seven multiple sclerosis cases but not in controls.

Topics: Antibodies, Monoclonal; Cross Reactions; Humans; Immunoenzyme Techniques; Immunoglobulins; Multiple Sclerosis; Myelin Basic Protein; Myelin Proteins; Myelin-Associated Glycoprotein; Nerve Fibers; Optic Nerve; Retinal Diseases; Retinal Ganglion Cells; Retinitis