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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...

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.

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Related Experiment Video

Updated: Jun 18, 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

Bidirectional plasticity in fast-spiking GABA circuits by visual experience.

Yoko Yazaki-Sugiyama¹, Siu Kang, Hideyuki Câteau

¹CREST, JST, Toyonaka, Osaka 560-0082, Japan.

|November 13, 2009

Summary

Brain plasticity relies on balanced excitation and inhibition. This study reveals inhibitory neurons initially favor the deprived eye, then the open eye, impacting visual cortex development.

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Last Updated: Jun 18, 2026

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Published on: September 20, 2024

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Published on: February 25, 2022

Area of Science:

Neuroscience
Neurobiology
Developmental Neuroscience

Background:

Experience-dependent brain plasticity is crucial for development.
Balanced excitation and inhibition are necessary for neural plasticity.
The role of specific neural circuits in plasticity remains unclear.

Purpose of the Study:

To investigate the contribution of individual circuit elements to ocular dominance plasticity.
To analyze the in vivo intracellular activity of fast-spiking cells during visual deprivation.
To understand the dynamic changes in inhibitory circuits during visual cortex development.

Main Methods:

Intracellular recordings in vivo from fast-spiking cells in juvenile mice.
Ocular dominance plasticity was induced by visual deprivation.
Intracellular pharmacology was used to assess GABAergic impact on pyramidal cells.

Main Results:

Fast-spiking cells showed an initial shift towards the occluded eye, followed by a late preference for the open eye.
This pattern is consistent with spike-timing-dependent plasticity rules for inhibitory neurons.
A dynamic switch in the impact of GABA (gamma-aminobutyric acid) on pyramidal cells was observed only in juvenile mice.

Conclusions:

Bidirectional recruitment of initially binocular GABAergic circuits may underlie experience-dependent plasticity.
Inhibitory interneurons play a dynamic and counterintuitive role in visual cortex plasticity.
Understanding these mechanisms is key to comprehending visual development and potential therapeutic interventions.