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Related Experiment Video

Updated: Jun 26, 2025

Generation of Oligodendrocytes and Oligodendrocyte-Conditioned Medium for Co-Culture Experiments

Generation of Oligodendrocytes and Oligodendrocyte-Conditioned Medium for Co-Culture Experiments

Published on: February 9, 2020

Dysregulated Cholinergic Signaling Inhibits Oligodendrocyte Maturation Following Demyelination.

Roopa Ravichandar¹, Farah Gadelkarim¹, Rupadevi Muthaiah²

¹Neuroscience Program, Jacob's School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York 14203.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience

|May 15, 2024

Summary

Dysregulated acetylcholine (ACh) levels hinder myelin repair in multiple sclerosis (MS). Increased ACh due to demyelination impairs oligodendrocyte differentiation, blocking remyelination. This study reveals ACh homeostasis disruption as a key factor in MS myelin repair failure.

Keywords:

acetylcholine butyrylcholinesterase remyelination

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Published on: February 17, 2016

Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Remyelination failure in multiple sclerosis (MS) involves oligodendrocyte progenitor cell (OPC) recruitment and differentiation issues.
Muscarinic receptor deletion improves OPC differentiation and remyelination, but the role of ligand-dependent signaling is unclear.

Purpose of the Study:

To investigate the hypothesis that altered acetylcholine (ACh) release during demyelination leads to ligand-mediated activation that impairs myelin repair.
To explore the contribution of ACh homeostasis dysregulation to remyelination failure in MS.

Main Methods:

Induction of chronic demyelination using cuprizone (CPZ) and lysolecithin in mice.
Measurement of ACh concentration and assessment of choline acetyltransferase (ChAT) and butyrylcholinesterase (BChE) expression.
Administration of neostigmine (cholinesterase inhibitor) to modulate ACh levels following lysolecithin-induced demyelination.

Main Results:

ACh concentration increased 2.5-fold following CPZ-induced demyelination.
Increased ChAT-GFP expression observed in neurons and astrocytes, indicating potential neuronal and astrocytic ACh release.
Decreased BChE expression linked to the loss of myelinating oligodendrocytes.
Neostigmine administration resulted in a dose-dependent decrease in mature oligodendrocyte density, without affecting OPC recruitment.

Conclusions:

Ligand-mediated activation of muscarinic receptors plays a functional role following demyelination.
Dysregulation of ACh homeostasis directly contributes to the failure of remyelination in MS.
Targeting ACh homeostasis may offer a therapeutic strategy for promoting myelin repair in demyelinating diseases.