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When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...
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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Synapse Dysfunctions in Multiple Sclerosis.

Karin Schwarz1, Frank Schmitz1

  • 1Department of Neuroanatomy, Institute of Anatomy and Cell Biology, Medical School, Saarland University, 66421 Homburg, Germany.

International Journal of Molecular Sciences
|January 21, 2023
PubMed
Summary
This summary is machine-generated.

Multiple sclerosis (MS) involves brain inflammation damaging grey matter synapses early, independent of white matter damage. This review explores how disturbed glia-synapse communication drives MS-related cognitive and mental symptoms.

Keywords:
astrocyteglutamateglutamate excitotoxicityionotropic glutamate receptorsmicrogliamultiple sclerosissynapsesynaptopathy

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Area of Science:

  • Neuroscience
  • Immunology
  • Neurology

Background:

  • Multiple sclerosis (MS) is a chronic central nervous system (CNS) disease affecting millions globally.
  • MS involves auto-reactive immune cells invading the brain, causing widespread neuroinflammation in both white and grey matter.
  • Neuroinflammation in MS grey matter leads to early synapse dysfunction, potentially causing cognitive and mental symptoms.

Purpose of the Study:

  • To review normal synapse/glia communication.
  • To summarize how this communication is disrupted in MS neuroinflammation.
  • To discuss mechanisms linking disturbed glia/synapse communication to MS pathology.

Main Methods:

  • Literature review of synapse-glia interactions in normal and MS conditions.
  • Analysis of neuroinflammatory mechanisms affecting grey matter synapses.
  • Discussion of excitotoxic damage and signaling imbalances.

Main Results:

  • Synapse dysfunction in MS grey matter occurs early and is independent of white matter demyelination.
  • Disturbed glia-synapse interactions and elevated neuroinflammation are central to MS pathology.
  • Glutamatergic excitotoxic synapse damage is a key mechanism in MS.

Conclusions:

  • Impaired glia-synapse communication is a critical factor in MS-related synapse dysfunction, signaling imbalance, and neurodegeneration.
  • Understanding these interactions is crucial for addressing cognitive and mental symptoms in MS.
  • Targeting glia-synapse communication may offer therapeutic strategies for MS.