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

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...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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...
Long-term Potentiation01:35

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Long-term Potentiation01:25

Long-term Potentiation

Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
LTP can occur when presynaptic neurons...
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...

You might also read

Related Articles

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

Sort by
Same author

Surviving microglia and nonmicroglial progenitors contribute to microglial repopulation following colony-stimulating factor 1 receptor inhibition.

Neuroreport·2026
Same author

A Comparative Analysis of iPSC, MSC, and 293T-Derived Exosomes for Parkinson's Disease Therapy.

International journal of molecular sciences·2026
Same author

Concurrent P-Selectin Targeting Nanoparticle Orchestrates Tumor-Immune Dynamics for Advanced Immunochemotherapy.

ACS nano·2026
Same author

3D-AI mouse behavior analysis system has the capability to detect abnormalities in R6/1 model mice with Huntington's disease during the pre-symptomatic phase.

Frontiers in psychiatry·2026
Same author

GluN2B-specific NMDAR positive allosteric modulation reverses cognitive and behavioral abnormalities in <i>Mecp2</i> and <i>Disc1</i> transgenic mice.

Science advances·2026
Same author

Activation of the supramammillary-dentate gyrus circuit enhances alertness and cognitive function in a rat model of ADHD.

Translational psychiatry·2025

Related Experiment Video

Updated: Jun 4, 2026

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke
07:00

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke

Published on: February 4, 2014

Stroke intervention pathways: NMDA receptors and beyond.

Ted Weita Lai1, Woei-Cherng Shyu, Yu Tian Wang

  • 1Brain Research Centre and Department of Medicine, University of British Columbia, Vancouver, Canada, V6T 2B5.

Trends in Molecular Medicine
|February 12, 2011
PubMed
Summary

New research explores N-methyl-D-aspartate receptors (NMDARs) in stroke. Understanding specific NMDAR pathways offers hope for developing effective neuroprotective stroke therapies with fewer side effects.

More Related Videos

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
04:48

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

Published on: July 10, 2018

Related Experiment Videos

Last Updated: Jun 4, 2026

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke
07:00

Excitotoxic Stimulation of Brain Microslices as an In vitro Model of Stroke

Published on: February 4, 2014

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate
04:48

A High-throughput Calcium-flux Assay to Study NMDA-receptors with Sensitivity to Glycine/D-serine and Glutamate

Published on: July 10, 2018

Area of Science:

  • Neuroscience
  • Pharmacology
  • Stroke Research

Background:

  • Excessive N-methyl-D-aspartate receptor (NMDAR) stimulation is linked to brain damage after stroke.
  • Previous clinical trials targeting NMDARs for stroke have been unsuccessful.

Purpose of the Study:

  • To review recent advancements in understanding NMDAR subpopulations and downstream effectors in stroke.
  • To highlight novel targets for developing improved NMDAR-based neuroprotective stroke therapies.

Main Methods:

  • Review of preclinical and clinical research on NMDARs in stroke.
  • Analysis of signaling pathways downstream of NMDARs involved in neuronal survival and death.

Main Results:

  • Identification of distinct NMDAR subpopulations with differential roles in neuronal fate.
  • Discovery of specific downstream signaling effectors mediating NMDAR-induced neurotoxicity or neuroprotection.

Conclusions:

  • Novel signaling pathways downstream of NMDARs present promising therapeutic targets for stroke.
  • Future stroke therapies may leverage specific NMDAR modulation for enhanced efficacy and reduced side effects.