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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...

Neuroplasticity

Neuroplasticity

Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

Plasticity

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...

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Related Experiment Video

Updated: Jul 19, 2026

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

Developmental switch from LTD to LTP in low frequency-induced plasticity.

Fabien Lanté¹, Mélanie Cavalier, Catherine Cohen-Solal

¹Laboratory Oxidative Stress and Neuroprotection, University Montpellier II, Montpellier, Cedex, France.

|October 4, 2006

Summary

Low-frequency stimulation in young rats induces long-term depression (LTD) via NMDA and mGlu5 receptors, switching to long-term potentiation (LTP) in adults. This synaptic plasticity demonstrates a developmental shift in the hippocampus.

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Standardized Induction and Assessment of Long-term Potentiation-like Cortical Plasticity Using Transcranial Magnetic Stimulation

Standardized Induction and Assessment of Long-term Potentiation-like Cortical Plasticity Using Transcranial Magnetic Stimulation

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Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Published on: August 11, 2019

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Last Updated: Jul 19, 2026

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

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Published on: September 20, 2024

Standardized Induction and Assessment of Long-term Potentiation-like Cortical Plasticity Using Transcranial Magnetic Stimulation

Standardized Induction and Assessment of Long-term Potentiation-like Cortical Plasticity Using Transcranial Magnetic Stimulation

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Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording

Published on: August 11, 2019

Area of Science:

Neuroscience
Synaptic Plasticity
Developmental Biology

Background:

Low-frequency stimulation (LFS) can induce long-term potentiation (LTP) in the adult hippocampus.
The developmental trajectory of LFS-induced synaptic plasticity remains incompletely understood.

Purpose of the Study:

To investigate the developmental profile of low-frequency stimulation (LFS)-induced plasticity in the rat hippocampus.
To elucidate the receptor mechanisms underlying LFS-induced long-term depression (LTD) during early development.

Main Methods:

Electrophysiological recordings in hippocampal slices from rats of different age groups (9-15, 17-21, and >25 days old).
Application of low-frequency stimulation (1 Hz) with varying durations.
Pharmacological manipulation using antagonists for N-methyl-D-aspartate (NMDA) and metabotropic glutamate 5 (mGlu5) receptors.

Main Results:

In young rats (9-15 days), 1 Hz stimulation induced LFS-LTD dependent on NMDA and mGlu5 receptors.
In adolescent rats (17-21 days), 1 Hz stimulation was ineffective or induced LTD with prolonged stimulation.
In adult rats (>25 days), 1 Hz stimulation induced LFS-LTP.
LFS-LTD occluded chemically induced LTDs, suggesting a shared postsynaptic mechanism involving NMDA and mGlu5 receptors.

Conclusions:

Synaptic plasticity induced by LFS undergoes a developmental switch from NMDA/mGlu5 receptor-dependent LTD in young rats to mGlu5 receptor-dependent LTP in adults.
A transient period exists in adolescent rats where LFS is ineffective, highlighting critical developmental windows for synaptic plasticity.