Neuron and Glia Interactions in Multiple Sclerosis: Focus on Ion Channels

Dear Colleagues,

The brain consists of two main cell classes—neurons and glial cells—both of which are essential components of the nervous system. These glial cells are astrocytes, oligodendrocytes, and microglia. In neuronal–glial interactions, each provides numerous mechanisms of support to neurons, such as increasing the capacity of signal transmission, compensating for excessive neurotransmitter release, maintaining ionic balance, building myelin sheath, metabolic support, and neuroimmunity.

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Although its detailed etiology has not sufficiently been elucidated, it is vital to discuss the interplay between experimental and clinical findings in disorders of the central nervous system in detail, as planned for this Special Issue. Particularly epidemiological MS studies showed that the risk for disease onset also includes genetic, epigenetic and environmental components.

It is well known that MS patients suffer from a multitude of clinical symptoms that reflect the lesion sites. Symptoms include impairments of motor behavior, sensory dysfunctions, ataxia, and visual disturbances.

Inflammatory infiltrates composed of auto-reactive T lymphocytes, B lymphocytes, and macrophages in the CNS of MS patients invade the brain and cause the selective destruction of myelin lamellae. Neuroinflammation triggers a harmful, complex, and multifaceted process not only in the white matter, but also in the gray matter of the brain. Neuroinflammation in gray matter causes synaptic dysfunction. Primary inflammatory demyelination causes axonal dysfunction and neuronal death, as well as the abnormal activation of glial cells and impaired synapse–glia interactions.

Current immunomodulatory therapies offer limited benefit to MS once it enters this irreversible progressive stage of the disease. Therefore, elucidating the mechanisms responsible for axonal loss is essential for the development of treatments to halt neurological decline in MS patients.

Oligodendrocyte progenitor cells (OPCs) differentiate into mature oligodendrocytes that migrate to the lesion site under demyelinating conditions and remyelinate damaged axons. However, due to the chronicity of the disease, there is a disruption in the OPC differentiation process. Moreover, OPCs are crucial players in neuronal–glial communication, as they receive synaptic input from neurons and express ion channels and neurotransmitter/neuromodulator receptors that control their maturation. Astrocytes and microglial cells are also equipped with a variety of receptors and ion channels that enable the precise sensing of environmental cues.

Ion channels in neuronal–glial interactions in MS are considered attractive therapeutic targets. Indeed, inward-rectifying potassium channel (Kir) and bi-pore domain potassium channels (K2P), transient receptor potential (TRP) channels, and ligand-gated and voltage-gated channels can all be found among its target group. Its modulations improve some symptoms of MS. However, the precise mechanism of action of ion-channel targeting compounds is often still unclear due to the broad expression of these channels on neurons, glia, and infiltrating immune cells.

This Special Issue aims to provide a platform for researchers to discuss their experimental and clinical findings or insights regarding all ion channels and related mechanisms involved in neuron–glia interactions in the pathogenesis of MS disease from the clinical point of view, including, but not limited to:

• MS disease pathogenesis;
• Animal models of MS disease;
• Microglia–neuron interactions and ion channels in MS;
• Neuroinflammation and ion channels in MS;
• Oligodendrocyte–neuron interactions and ion channels in MS;
• Astrocyte–blood vessel–neuron interactions and ion channels in MS;
• Oligodendrocyte apoptosis and myelin damage;
• Myelin damage and TRP channels;
• Myelin damage and K+ channels.

Dr. Bilal ÇİĞ
Prof. Dr. Thomas Müller
Guest Editors

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• MS disease pathogenesis
• animal models of MS disease
• microglia–neuron interactions and ion channels in MS
• neuroinflammation and ion channels in MS
• oligodendrocyte–neuron interactions and ion channels in MS
• astrocyte–blood vessel–neuron interactions and ion channels in MS
• oligodendrocyte apoptosis and myelin damage
• myelin damage and TRP channels
• myelin damage and K+ channels