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In vivo modulation of oligodendrocyte function by an anti-receptor antibody
J A Cohen1, R C Sergott, W V Williams
1Department of Neurology, University of Pennsylvania, Philadelphia 19104-4283.
Abstract:
The receptor for reovirus serotype 3 (Reo3R) is biochemically, pharmacologically, and antigenically related to the adrenergic receptors. Previous studies have demonstrated that anti-Reo3R antibodies and Reo3R-binding peptides alter oligodendrocyte differentiation in culture. In the present studies, antibodies and peptides that bind the Reo3R were found to alter myelin morphology in vivo. Microinjection of purified anti-Reo3R antibody into guinea pig optic nerves produced expansion of the adaxonal oligodendrocyte cytoplasm, separation of myelin lamellae, widening of Schmidt-Lanterman clefts, myelin vesiculation, and demyelination. A divalent Reo3R-binding peptide reproduced some of these changes. Anti-Reo3R antibodies and Reo3R-binding peptides alter oligodendrocyte function in vivo resulting in myelin changes. These effects appear to be mediated directly by Reo3R perturbation, at least in part, rather than through activation of additional effector mechanisms.
Insights
Antibodies targeting the reovirus serotype 3 receptor (Reo3R) disrupt myelin structure in vivo. This research reveals Reo3R
Area of Science:
- Neuroscience
- Cell Biology
- Virology
Background:
- The reovirus serotype 3 receptor (Reo3R) shares similarities with adrenergic receptors.
- Previous research indicated Reo3R modulation affects oligodendrocyte differentiation in vitro.
Purpose of the Study:
- To investigate the in vivo effects of Reo3R-binding antibodies and peptides on myelin morphology.
- To determine if Reo3R perturbation directly impacts oligodendrocyte function and myelin integrity.
Main Methods:
- Microinjection of anti-Reo3R antibodies into guinea pig optic nerves.
- Administration of divalent Reo3R-binding peptides.
- Microscopic analysis of myelin structure and oligodendrocyte morphology.
Main Results:
- Anti-Reo3R antibody injection caused significant myelin alterations, including lamellar separation, widened clefts, vesiculation, and demyelination.
- Oligodendrocyte cytoplasm expansion was observed.
- Reo3R-binding peptides partially replicated these myelin changes.
Conclusions:
- Reo3R antibodies and peptides alter oligodendrocyte function in vivo, leading to myelin pathology.
- These myelin changes are likely mediated directly by Reo3R perturbation.