Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
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...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Cytomorphometric and Clinical Analysis of the Effects of Azithromycin and Platelet-Rich Fibrin on Wound Healing After Surgical Removal of an Impacted Mandibular Third Molar.

Journal of functional biomaterials·2026
Same author

Activation of Intestinal Type 3 Innate Lymphoid Cells and Regulatory T Cells Through Free Fatty Acid Receptor 2 Ameliorates Type 1 Diabetes in Mice.

Diabetes·2026
Same author

A Novel System for Physiological Signal Monitoring and Health-Informed Electrotactile Feedback for First Responders.

Sensors (Basel, Switzerland)·2026
Same author

Topical Polyherbal Phytopreparation Reduces Gingival Inflammation: Evidence from a Randomized Controlled Clinical Study Supported by In Silico Analysis.

Pharmaceuticals (Basel, Switzerland)·2026
Same author

Marginal adaptation and microleakage of resin-based composite provisional crowns fabricated by different techniques and materials.

European journal of oral sciences·2026
Same author

A Comparative Analysis of Differences in Salivary hBD-2 Levels and Their Correlation with Dental Caries and Unstimulated Saliva pH in Children with Primary and Permanent Dentition.

Diagnostics (Basel, Switzerland)·2026

Related Experiment Video

Updated: May 16, 2026

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models
10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

Multiple sclerosis and glutamate excitotoxicity.

Milos Kostic1, Nikola Zivkovic, Ivana Stojanovic

  • 1Departement of Immunology, Faculty of Medicine, University of Nis, 18000 Nis, Serbia. milosh.kostic@hotmail.com

Reviews in the Neurosciences
|November 16, 2012
PubMed
Summary
This summary is machine-generated.

Glutamate excitotoxicity, involving excessive glutamate signaling, is a key factor in multiple sclerosis (MS) neurodegeneration beyond inflammation. Understanding this mechanism is crucial for MS treatment strategies.

More Related Videos

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
06:36

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices

Published on: February 5, 2015

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
08:17

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis

Published on: February 23, 2024

Related Experiment Videos

Last Updated: May 16, 2026

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models
10:46

Using Enzyme-based Biosensors to Measure Tonic and Phasic Glutamate in Alzheimer's Mouse Models

Published on: May 3, 2017

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices
06:36

An Ex vivo Model of an Oligodendrocyte-directed T-Cell Attack in Acute Brain Slices

Published on: February 5, 2015

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis
08:17

Scoring Central Nervous System Inflammation, Demyelination, and Axon Injury in Experimental Autoimmune Encephalomyelitis

Published on: February 23, 2024

Area of Science:

  • Neuroscience
  • Neuroimmunology
  • Neurodegeneration

Background:

  • Multiple sclerosis (MS) was historically viewed primarily through the lens of neuroinflammation.
  • Emerging evidence highlights inflammation-independent neurodegenerative processes in MS, including mitochondrial dysfunction, iron deposition, and oxidative stress.

Purpose of the Study:

  • To explore glutamate excitotoxicity as a potential link between inflammatory and neurodegenerative pathways in multiple sclerosis.
  • To revise current understanding of elevated extracellular glutamate, receptor alterations, and transporter/enzyme changes in MS.

Main Methods:

  • Review and synthesis of existing data on glutamate excitotoxicity in the context of multiple sclerosis.
  • Analysis of the role of glutamate homeostasis disruption in central nervous system (CNS) damage in MS.

Main Results:

  • Glutamate excitotoxicity, caused by excessive glutamate receptor activation, induces cell death and may bridge inflammatory and neurodegenerative aspects of MS.
  • Disturbances in glutamate homeostasis impact CNS cell communication and function, contributing to diverse pathological events in MS.

Conclusions:

  • Glutamate excitotoxicity is a significant mechanism of CNS damage in multiple sclerosis.
  • Further research is needed on glutamate sources, receptor/transporter alterations, and the molecular mechanisms of excitotoxic damage in MS.