Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Long-term Depression

Long-term Depression

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 time, all...

Long-term Depression

Long-term Depression

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.

Long-term Potentiation

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 Potentiation

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...

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

You might also read

Related Articles

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

Sort by

Same author

Alteration of cellular representation in the central amygdala mediates stress-induced analgesia in mice.

Neuron·2026

Same author

Evolutionary convergence and divergence of hippocampal cytoarchitecture between rodents and primates revealed by single-cell spatial transcriptomics.

National science review·2026

Same author

Transcriptomic and spatial organization of mouse spinal cord projection neurons.

Cell reports·2025

Same author

Sympathetic nerve dysfunction exacerbates skin inflammation in atopic dermatitis.

The Journal of allergy and clinical immunology·2025

Same author

Author Correction: Projectome-based characterization of hypothalamic peptidergic neurons in male mice.

Nature neuroscience·2025

Same author

Central neural circuits underlying itch sensation.

Nature reviews. Neuroscience·2025

Search research articles

Related Experiment Video

Updated: Jun 4, 2026

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

Published on: August 7, 2019

Receptor saturation controls short-term synaptic plasticity at corticothalamic synapses.

Yan-Gang Sun¹, Michael Beierlein

¹Department of Neurobiology and Anatomy, University of Texas Medical School, 6431 Fannin, Houston, TX 77030, USA.

Journal of Neurophysiology

|February 18, 2011

Summary

Short-term synaptic enhancement at corticothalamic (CT) synapses is controlled by postsynaptic receptor saturation. Relieving this saturation boosts synaptic plasticity, revealing a key mechanism in sensory processing.

More Related Videos

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Published on: January 1, 2018

Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus

Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus

Published on: September 20, 2024

Related Experiment Videos

Last Updated: Jun 4, 2026

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

Electrophysiological Investigations of Retinogeniculate and Corticogeniculate Synapse Function

Published on: August 7, 2019

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Recording Synaptic Plasticity in Acute Hippocampal Slices Maintained in a Small-volume Recycling-, Perfusion-, and Submersion-type Chamber System

Published on: January 1, 2018

Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus

Inducing Long-Term Plasticity of Intrinsic Neuronal Excitability in Neurons of the Dorsal Lateral Geniculate Nucleus

Published on: September 20, 2024

Area of Science:

Neuroscience
Synaptic Plasticity
Sensory Processing

Background:

Layer 6 corticothalamic (CT) neurons provide major excitatory input to thalamic relay cells, enabling neocortical control over sensory information processing.
CT synapses exhibit use-dependent short- and long-term enhancement, partly due to increased neurotransmitter release probability.
The interplay between multivesicular release (MVR), postsynaptic receptor saturation, and short-term plasticity at CT synapses remains unclear.

Purpose of the Study:

To investigate the roles of postsynaptic receptor saturation and multivesicular release in short-term plasticity at CT synapses.
To examine how relieving postsynaptic saturation affects synaptic enhancement, specifically facilitation and augmentation.

Main Methods:

Electrophysiological recordings from CT synapses onto relay neurons in the ventrobasal nucleus of the mouse thalamus.
Utilized the low-affinity antagonist γ-D-glutamylglycine to alleviate postsynaptic AMPA receptor saturation.
Assessed changes in synaptic facilitation and augmentation under conditions of relieved receptor saturation.

Main Results:

Blocking postsynaptic DL-α-amino-3-hydroxy-5-methylisox azole-propionic acid (AMPA) receptor saturation with γ-D-glutamylglycine significantly increased the magnitude of both facilitation and augmentation.
Postsynaptic receptor saturation was observed for both AMPA and N-methyl-D-aspartate receptors.
AMPA receptor desensitization did not substantially impact short-term plasticity.

Conclusions:

Activity-dependent increases in synaptic strength at CT synapses are significantly modulated by postsynaptic receptor saturation.
Postsynaptic factors, particularly receptor saturation, play a crucial role in regulating short-term plasticity at these critical sensory processing synapses.