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Exp Neurol. 2017 Sep;295:18-22. doi: 10.1016/j.expneurol.2017.05.004. Epub 2017 May 11.

Functional connectivity alterations in a murine model of optic neuritis.

Author information

1
Department of Radiology, Washington University in St. Louis School of Medicine, United States.
2
Department of Neurology, Washington University in St. Louis School of Medicine, United States.
3
Department of Ophthalmology, Washington University in St. Louis School of Medicine, United States.
4
Department of Radiology, Washington University in St. Louis School of Medicine, United States; Department of Neurology, Washington University in St. Louis School of Medicine, United States.
5
Department of Neurology, Washington University in St. Louis School of Medicine, United States; Department of Pathology & Immunology, Washington University in St. Louis School of Medicine, United States. Electronic address: wug@neuro.wustl.edu.

Abstract

The basis for neuronal dysfunction following inflammatory demyelination of the central nervous system (CNS) remains poorly understood. We characterized the network response to white matter injury in the anterior visual pathway using an experimental model of optic neuritis (ON), as ON is often an early manifestation of immune-mediated CNS demyelination in multiple sclerosis (MS). Optical intrinsic signal imaging was performed before and after the induction of ON in mice to measure changes in cortical network functional connectivity. We observed a greater loss of connectivity between homotopic visual cortices in ON mice compared to controls. Further, decreases in homotopic visual cortex connectivity were associated with visual acuity loss in ON mice. These results demonstrate that network connectivity changes resulting from ON can be modeled in an experimental murine system. Future studies will identify the mechanisms that cause neuronal dysfunction due to white matter injury seen in MS.

KEYWORDS:

Demyelination; Functional connectivity; Multiple sclerosis; Optic neuritis; Optical imaging; Visual cortex

PMID:
28502610
PMCID:
PMC5657240
[Available on 2018-09-01]
DOI:
10.1016/j.expneurol.2017.05.004
[Indexed for MEDLINE]

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