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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, RESULTS. Meshes: Animals, Basic Helix-Loop-Helix Transcription Factors, Bromodeoxyuridine, Cell Movement, Cell Proliferation, Demyelinating Diseases, Evoked Potentials, Visual, GPI-Linked Proteins, Gene Expression Regulation, Injections, Intraventricular, Lysophosphatidylcholines, Male, Mice, Mice, Inbred C57BL, Microinjections, Myelin Proteins, Myelin Sheath, Nerve Tissue Proteins, Nogo Receptor 1, Oligodendrocyte Transcription Factor 2, Optic Chiasm, RNA, Small Interfering, Receptors, Cell Surface, Recovery of Function, Stem Cells, Time Factors.
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Does nogo receptor inhibition enhance functional recovery following lysolecithin-induced demyelination in mouse optic chiasm? Context: Inhibitory factors have been implicated in the failure of remyelination in demyelinating diseases. Myelin associated inhibitors act through a common receptor called Nogo receptor (NgR) that plays critical inhibitory roles in CNS plasticity. Here we investigated the effects of abrogating NgR inhibition in a non-immune model of focal demyelination in adult mouse optic chiasm. A focal area of demyelination was induced in adult mouse optic chiasm by microinjection of lysolecithin. To knock down NgR levels, siRNAs against NgR were intracerebroventricularly administered via a permanent cannula over 14 days, Functional changes were monitored by electrophysiological recording of latency of visual evoked potentials (VEPs). Histological analysis was carried out 3, 7 and 14 days post demyelination lesion. To assess the effect of NgR inhibition on precursor cell repopulation, BrdU was administered to the animals prior to the demyelination induction. Inhibition of NgR significantly restored VEPs responses following optic chiasm demyelination. These findings were confirmed histologically by myelin specific staining. siNgR application resulted in a smaller lesion size compared to control. NgR inhibition significantly increased the numbers of BrdU+/Olig2+ progenitor cells in the lesioned area and in the neurogenic zone of the third ventricle. These progenitor cells (Olig2+ or GFAP+) migrated away from this area as a function of time.
assistant
Our results show that inhibition of NgR facilitate myelin repair in the demyelinated chiasm, with enhanced recruitment of proliferating cells to the lesion site. Thus, antagonizing NgR function could have therapeutic potential for demyelinating disorders such as Multiple Sclerosis. Final Decision: yes