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Related Concept Videos

Long-term Potentiation01:25

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 Potentiation01:35

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.
Chemical Synapses01:26

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 Synapses01:26

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...
Integration of Synaptic Events01:28

Integration of Synaptic Events

Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

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...

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Related Experiment Video

Updated: Jun 11, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

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Published on: March 20, 2014

Metaplasticity at single glutamatergic synapses.

Ming-Chia Lee1, Ryohei Yasuda, Michael D Ehlers

  • 1Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.

Neuron
|July 13, 2010
PubMed
Summary
This summary is machine-generated.

Spontaneous glutamate release adjusts synaptic plasticity thresholds by altering NMDA receptor function at individual synapses. This local mechanism, a novel form of metaplasticity, primes or prevents synaptic potentiation.

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Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration
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Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala
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Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala

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Related Experiment Videos

Last Updated: Jun 11, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates

Published on: March 20, 2014

Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration
07:08

Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration

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Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala
09:49

Combined Optogenetic and Freeze-fracture Replica Immunolabeling to Examine Input-specific Arrangement of Glutamate Receptors in the Mouse Amygdala

Published on: April 15, 2016

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Metaplasticity

Background:

  • Neuronal network function depends on Hebbian plasticity and metaplasticity.
  • Rules governing synaptic metaplasticity are not well understood.
  • NMDA receptors play a crucial role in synaptic plasticity.

Purpose of the Study:

  • To investigate the rules governing synaptic metaplasticity.
  • To identify mechanisms that regulate the threshold for synaptic plasticity.
  • To explore the role of NMDA receptors in metaplasticity.

Main Methods:

  • Studied NMDA receptor function at single dendritic spines.
  • Manipulated neurotransmitter release and measured receptor currents.
  • Assessed calcium transients and synaptic potentiation thresholds.
  • Investigated the role of spontaneous glutamate release and action potentials.

Main Results:

  • Demonstrated a subunit-specific switch in NMDA receptors at single synapses.
  • Prolonged suppression of neurotransmitter release enhanced NMDA receptor currents and calcium transients.
  • Showed that spontaneous glutamate release, not action potentials, drives this switch.
  • Inactivated synapses exhibited a lower threshold for long-term potentiation and spine growth.

Conclusions:

  • Spontaneous glutamate release locally regulates NMDA receptors to adjust synaptic plasticity thresholds.
  • This represents a novel, spatially delimited form of synaptic metaplasticity.
  • Findings provide new insights into the homeostatic regulation of neuronal function.