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

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

910
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.
910
Role of Neurotransmitters in Memory01:23

Role of Neurotransmitters in Memory

3.0K
Neurotransmitters are integral to the brain's communication system, enabling neurons to transmit signals across synapses. This chemical exchange underpins various cognitive functions, including memory processes. The role of neurotransmitters in memory is multifaceted, influencing the encoding, consolidation, and retrieval of memories through their action on different neural circuits.
 Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
3.0K
Long-term Depression01:03

Long-term Depression

3.6K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over...
3.6K
Long-term Depression01:05

Long-term Depression

33.9K
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
33.9K
Antiepileptic Drugs: Glutamate Antagonists01:14

Antiepileptic Drugs: Glutamate Antagonists

1.3K
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...
1.3K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

5.0K
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...
5.0K

You might also read

Related Articles

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

Sort by
Same author

Sex- and experience-dependent regulation of synaptic protein turnover.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Human-in-the-loop governance of artificial intelligence in cardiology: From ethical principles to operational paradigms.

Indian heart journal·2026
Same author

Dynamic visualization of physiological CaMKII activity using sensitive FRET biosensors.

bioRxiv : the preprint server for biology·2026
Same author

European Journal of Heart Failure International Expert Position Paper Utilisation, Optimisation, and Clinical Benefits of Steroidal Mineralocorticoid Receptor Antagonists in Heart Failure with a Reduced Ejection Fraction.

European journal of heart failure·2026
Same author

Prediction of wear outcomes and mechanical characterization of innovative SiO<sub>2</sub> incorporated aluminium matrix composites.

Scientific reports·2026
Same author

Safety and efficacy of a novel traction balloon technique for guide-extension advancement in complex coronary interventions: a case series.

American journal of cardiovascular disease·2026

Related Experiment Video

Updated: Apr 14, 2026

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

6.7K

Glutamate synapses in human cognitive disorders.

Lenora Volk1, Shu-Ling Chiu, Kamal Sharma

  • 1Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205;

Annual Review of Neuroscience
|April 22, 2015
PubMed
Summary

Altered glutamatergic synapse function is implicated in intellectual disability (ID), autism spectrum disorder (ASD), and schizophrenia (SCZ). Genetic and animal studies reveal shared neuropathology in these neurodevelopmental disorders.

Keywords:
autismexcitatoryintellectual disabilityneurodevelopmentalplasticityschizophrenia

More Related Videos

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

11.9K
A High-content Assay for Monitoring AMPA Receptor Trafficking
10:34

A High-content Assay for Monitoring AMPA Receptor Trafficking

Published on: January 28, 2019

8.2K

Related Experiment Videos

Last Updated: Apr 14, 2026

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
08:27

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice

Published on: March 11, 2020

6.7K
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

11.9K
A High-content Assay for Monitoring AMPA Receptor Trafficking
10:34

A High-content Assay for Monitoring AMPA Receptor Trafficking

Published on: January 28, 2019

8.2K

Area of Science:

  • Neuroscience
  • Genetics
  • Cognitive Disorders

Background:

  • Cognitive disorders like intellectual disability (ID), autism spectrum disorder (ASD), and schizophrenia (SCZ) share common pathologies.
  • Alterations in glutamatergic synapse structure and function are increasingly recognized as a unifying factor.

Purpose of the Study:

  • To review genetic and animal model evidence linking aberrant glutamatergic synapse function to ID, ASD, and SCZ.
  • To highlight candidate genes and their functional consequences in these neurodevelopmental disorders.

Main Methods:

  • Review of human genetic association studies.
  • Analysis of data from animal models of neurodevelopmental disorders.
  • Examination of genetic and phenotypic evidence for altered glutamate signaling.

Main Results:

  • Evidence supports a role for altered excitatory synapse function in the etiology of ID, ASD, and SCZ.
  • Pathology appears to stem from altered neural microstructure, function, and wiring, not gross neuronal changes.
  • Specific candidate genes affecting glutamatergic synapse function are identified.

Conclusions:

  • Intellectual disability, autism spectrum disorder, and schizophrenia may share a common underlying neuropathy centered on excitatory synapse dysfunction.
  • Understanding these shared mechanisms offers potential for novel therapeutic strategies.