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.

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...

The Synapse

The Synapse

Neurons communicate with one another by passing on their electrical signals to other neurons. A synapse is the location where two neurons meet to exchange signals. At the synapse, the neuron that sends the signal is called the presynaptic cell, while the neuron that receives the message is called the postsynaptic cell. Note that most neurons can be both presynaptic and postsynaptic, as they both transmit and receive information.

You might also read

Related Articles

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

Sort by

Same author

Sparseness facilitates image encoding across visuo-frontal networks in freely moving macaque.

Nature communications·2026

Same author

Unsupervised learning of temporal regularities in visual cortical populations.

Nature communications·2025

Same author

Optogenetic modulation of long-range cortical circuits in awake nonhuman primates.

Nature protocols·2025

Same author

NREM sleep improves behavioral performance by desynchronizing cortical circuits.

Science (New York, N.Y.)·2024

Same author

Publisher Correction: Visuo-frontal interactions during social learning in freely moving macaques.

Nature·2024

Same author

Population coding of strategic variables during foraging in freely moving macaques.

Nature neuroscience·2024

Search research articles

Related Experiment Video

Updated: Jul 13, 2026

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

Asymmetric synaptic depression in cortical networks.

Mircea I Chelaru¹, Valentin Dragoi

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

Cerebral Cortex (New York, N.Y. : 1991)

|August 19, 2007

Summary

Asymmetric synaptic depression, where excitatory synapses depress more than inhibitory ones, enhances neural circuit sensitivity. This differential depression improves stimulus coding by adjusting response gain in cortical networks.

More Related Videos

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

Published on: July 22, 2022

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Related Experiment Videos

Last Updated: Jul 13, 2026

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

DetectSyn: A Rapid, Unbiased Fluorescent Method to Detect Changes in Synapse Density

Published on: July 22, 2022

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

Area of Science:

Neuroscience
Computational Neuroscience
Systems Neuroscience

Background:

Synaptic depression is crucial for regulating excitation-inhibition balance in cortical networks.
Intracortical synapses exhibit asymmetric depression, with inhibitory synapses depressing less than excitatory ones.

Purpose of the Study:

To investigate the functional impact of asymmetric synaptic depression on cortical circuit dynamics.
To elucidate how differential synaptic depression influences stimulus coding and network sensitivity.

Main Methods:

Modeling recurrent interactions between orientation-selective neurons in the primary visual cortex (V1).
Analytical examination of synaptic depression effects on neural responses and network gain.

Main Results:

Despite greater depression of excitatory synapses, their responses are reduced less than inhibitory ones, leading to increased overall response gain.
Asymmetric synaptic depression actively contributes to selective gain control in visual cortical circuits.

Conclusions:

Differential synaptic depression provides a mechanism for dynamic gain and sensitivity shifts in cortical circuits.
This process enhances V1 neuron responses and sensitivity to infrequent stimuli while attenuating them for frequent stimuli, aligning with experimental observations.