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Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...

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Related Experiment Video

Updated: May 19, 2026

A Simple Cell-based Immunofluorescence Assay to Detect Autoantibody Against the N-Methyl-D-Aspartate (NMDA) Receptor in Blood
07:20

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Published on: January 9, 2018

Abnormal NMDA receptor function exacerbates experimental autoimmune encephalomyelitis.

G Grasselli1, S Rossi, A Musella

  • 1Fondazione Santa Lucia/Centro Europeo per la Ricerca sul Cervello (CERC), Università Tor Vergata, Rome, Italy.

British Journal of Pharmacology
|August 29, 2012
PubMed
Summary
This summary is machine-generated.

Overactive N-methyl-D-aspartate (NMDA) receptors increase glutamate release and worsen multiple sclerosis (MS) symptoms in EAE mice. Blocking NMDA receptors improved disease course, suggesting NMDA receptor antagonists for MS neuroprotection.

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Glutamate neurotransmission is altered in multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE).
  • EAE is characterized by increased glutamate transmission and AMPA receptor upregulation.
  • The specific role of N-methyl-D-aspartate (NMDA) receptors in EAE-induced synaptic changes remains unclear.

Purpose of the Study:

  • To investigate the contribution of NMDA receptors to glutamate transmission alterations in EAE.
  • To assess the impact of NMDA receptor activity on EAE disease severity.
  • To explore NMDA receptor signaling as a potential therapeutic target for MS.

Main Methods:

  • Neurophysiological recordings to assess synaptic transmission.
  • Morphological and Western blot analyses for receptor and cellular changes.
  • Metabolic assessments using NAD(P)H autofluorescence to evaluate mitochondrial function.
  • Clinical scoring to monitor disease progression in EAE mice.

Main Results:

  • EAE mice exhibited increased glutamate release dependent on NMDA receptor activity.
  • Presynaptic NMDA receptors were found to be overactive in EAE, enhancing glutamate release via sodium channels.
  • EAE induced mitochondrial dysfunction, linked to glutamate and NMDA receptor activity.
  • Pharmacological blockade of NMDA receptors ameliorated synaptic deficits and clinical symptoms in EAE mice.

Conclusions:

  • NMDA receptor signaling is sensitized in EAE and contributes to disease progression.
  • Targeting NMDA receptors may offer a neuroprotective strategy for multiple sclerosis.
  • These findings highlight the potential of NMDA receptor antagonists in MS treatment.