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

Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

310
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...
310
Sedatives and Hypnotics Drugs: Miscellaneous Agents01:17

Sedatives and Hypnotics Drugs: Miscellaneous Agents

163
Sedatives and hypnotics encompass a wide range of substances, each with its unique mechanism of action, uses, and potential adverse effects.
Melatonin congeners like ramelteon (Rozerem) and tasimelteon (Hetlioz) selectively bind to melatonin receptors (MT1 and MT2) and thus mimic the actions of melatonin, a hormone that regulates sleep-wake cycles. Tasimelteon is primarily used for non-24-hour sleep-wake disorder, common in blind patients. They are also used to treat conditions like insomnia...
163
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

2.2K
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...
2.2K
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

114
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
114
Parenteral Anesthetics: Overview01:24

Parenteral Anesthetics: Overview

114
Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
114
Sedatives and Hypnotics: Overview01:23

Sedatives and Hypnotics: Overview

325
Sedatives are drugs that alleviate anxiety, while hypnotics induce sleep. Both classes of medication suppress neuronal activity, leading to a calming effect for sedatives and facilitating sleep for hypnotics.
Sedative-hypnotics are categorized into barbiturates, benzodiazepines (BZDs), and non-benzodiazepines or Z-drugs. These drugs work by suppressing central nervous system activity, and this suppression is dose-dependent. Older sedative medications, like barbiturates, follow a linear curve in...
325

You might also read

Related Articles

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

Sort by
Same author

Immune checkpoint inhibitor neurotoxicity: long-term outcomes with focus on 1-year neurological sequelae.

Journal for immunotherapy of cancer·2026
Same author

Isolated Peripheral Nervous System Presentation in Ma/Ma2-Associated Autoimmunity.

Neurology(R) neuroimmunology & neuroinflammation·2026
Same author

Vascular and mesenchymal signatures of breast cancers associated with Yo and Ri paraneoplastic syndrome.

Breast cancer research : BCR·2026
Same author

AEG-AESPANC-OPGE-SIED-SPG Ibero-Latin American Guidelines on Acute Pancreatitis (iLATAM-AP).

United European gastroenterology journal·2026
Same author

Alternative diagnoses of suspected paraneoplastic neurological syndromes: a population-based study.

Journal of neurology·2026
Same author

Pathogenic Role of FGFR3 Autoantibodies in Small Fiber Neuropathy.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Related Experiment Video

Updated: Jun 19, 2025

Horizontal Hippocampal Slices of the Mouse Brain
08:59

Horizontal Hippocampal Slices of the Mouse Brain

Published on: September 22, 2020

18.1K

Ketamine alleviates NMDA receptor hypofunction through synaptic trapping.

Frédéric Villéga1, Alexandra Fernandes2, Julie Jézéquel2

  • 1University of Bordeaux, CNRS, Interdisciplinary Institute for Neuroscience, IINS UMR 5297, 33000 Bordeaux, France; Department of Pediatric Neurology, CIC-1401, University Children's Hospital of Bordeaux, Bordeaux, France.

Neuron
|July 24, 2024
PubMed
Summary

Ketamine enhances N-methyl-D-aspartate glutamate receptor (NMDAR) trapping at synapses, which can counteract receptor loss caused by anti-NMDAR encephalitis and improve cognitive functions.

Keywords:
NMDA receptorantagonistautoimmunitybehaviorcell imaginghippocampusneuropsychiatrysingle nanoparticle trackingsurface diffusion

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

9.2K
Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
07:52

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents

Published on: June 2, 2015

11.9K

Related Experiment Videos

Last Updated: Jun 19, 2025

Horizontal Hippocampal Slices of the Mouse Brain
08:59

Horizontal Hippocampal Slices of the Mouse Brain

Published on: September 22, 2020

18.1K
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

9.2K
Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
07:52

Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents

Published on: June 2, 2015

11.9K

Area of Science:

  • Neuroscience
  • Neuropharmacology
  • Synaptic Plasticity

Background:

  • N-methyl-D-aspartate glutamate receptor (NMDAR) synaptic trapping is crucial for regulating excitatory neurotransmission and cognitive functions.
  • NMDAR synaptic destabilization is linked to neurological and psychiatric disorders, but therapeutic modulation of synaptic trapping remains challenging.

Purpose of the Study:

  • To investigate how ketamine (KET) and other NMDAR open channel blockers (OCBs) affect NMDAR synaptic trapping.
  • To determine if enhanced NMDAR trapping can mitigate deficits caused by autoantibodies in anti-NMDAR encephalitis.

Main Methods:

  • Examined the interaction between NMDAR and PDZ-domain scaffolding proteins upon OCB treatment.
  • Assessed the impact of KET-induced trapping enhancement on synaptic receptor levels in an anti-NMDAR encephalitis model.
  • Evaluated NMDAR-mediated CaMKII signaling and behavioral outcomes, including anxiety and sensorimotor gating.

Main Results:

  • Ketamine and other OCBs promote NMDAR interactions with PDZ-domain proteins, enhancing synaptic trapping.
  • KET-enhanced trapping counteracted synaptic receptor depletion induced by anti-NMDAR encephalitis autoantibodies.
  • Preventing synaptic depletion restored NMDAR-mediated CaMKII signaling and ameliorated behavioral deficits.

Conclusions:

  • OCBs exert an unexpected effect by enhancing NMDAR synaptic anchoring.
  • Targeting NMDAR receptor anchoring presents a potential therapeutic strategy for NMDAR-related synaptopathies.