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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.

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...

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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...

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...

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Related Experiment Video

Updated: May 17, 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

Short-term ionic plasticity at GABAergic synapses.

Joseph V Raimondo¹, Henry Markram, Colin J Akerman

¹Akerman Lab, Department of Pharmacology, Oxford University Oxford, Oxfordshire, UK.

Frontiers in Synaptic Neuroscience

|October 23, 2012

Summary

This summary is machine-generated.

Short-term ionic plasticity modifies brain inhibition by altering the driving force on γ-Aminobutyric acid (GABA) receptors. This activity-dependent process impacts inhibitory synapse function and neural network dynamics.

Keywords:

EGABA GABA GABAA receptors chloride pH reversal potential short-term ionic plasticity synaptic transmission

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

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Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

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Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABAA Receptors

Inhibitory Synapse Formation in a Co-culture Model Incorporating GABAergic Medium Spiny Neurons and HEK293 Cells Stably Expressing GABA_A Receptors

Published on: November 14, 2014

Area of Science:

Neuroscience
Synaptic Plasticity
Neurophysiology

Background:

Fast synaptic inhibition in the brain relies on GABA release and postsynaptic GABA receptor activation.
Plasticity mechanisms are increasingly recognized at inhibitory synapses, operating across various timescales.

Purpose of the Study:

To examine activity-dependent short-term ionic plasticity unique to GABAergic transmission.
To explore the underlying mechanisms, occurrence, and impact of this plasticity on network activity.

Main Methods:

Investigated changes in the ionic driving force at postsynaptic GABA receptors.
Analyzed the influence of synaptic activity history, synapse location, and postsynaptic ion regulation.

Main Results:

Identified short-lasting changes in the ionic driving force for postsynaptic GABA receptors.
Demonstrated that these changes are directly related to prior synaptic activity.

Conclusions:

Short-term ionic plasticity is a key feature of GABAergic transmission.
This plasticity is influenced by cellular and synaptic factors and affects overall neural network function.