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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...

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.

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...

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Related Experiment Video

Updated: Jul 5, 2026

Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice

Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice

Published on: November 29, 2013

MGluR5 mediates the interaction between late-LTP, network activity, and learning.

Arthur Bikbaev¹, Sergey Neyman, Richard Teke Ngomba

¹Department of Experimental Neurophysiology, Medical Faculty, Ruhr University Bochum, Bochum, Germany.

|May 15, 2008

Summary

Blocking metabotropic glutamate receptor 5 (mGluR5) impairs spatial memory by altering hippocampal synaptic plasticity and network activity. Restoring metabotropic glutamate receptor 1 (mGluR1) function partially reverses these effects, highlighting mGluR5

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Last Updated: Jul 5, 2026

Long-term Potentiation of Perforant Pathway-dentate Gyrus Synapse in Freely Behaving Mice

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Published on: November 29, 2013

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

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Area of Science:

Neuroscience
Molecular Biology
Cognitive Science

Background:

Metabotropic glutamate receptors (mGluRs), particularly mGluR5, play a crucial role in regulating hippocampal synaptic plasticity and learning.
Understanding the precise mechanisms of mGluR5 modulation is essential for developing therapeutic strategies for memory disorders.

Purpose of the Study:

To investigate the mechanisms by which mGluR5 influences hippocampal synaptic plasticity and spatial memory.
To elucidate the role of mGluR1 in mediating the effects of mGluR5 blockade.

Main Methods:

Prolonged pharmacological blockade of mGluR5 using MPEP.
Assessment of spatial memory, hippocampal long-term potentiation (LTP) in dentate gyrus and CA1 regions, mGluR1a expression, and network oscillations (theta and gamma).
CA3-lesioning to investigate the origin of CA1-LTP changes.

Main Results:

MPEP treatment profoundly impaired spatial memory.
mGluR5 blockade reduced mGluR1a expression and impaired dentate gyrus LTP, while enhancing CA1-LTP.
Theta and gamma oscillations in the dentate gyrus were suppressed by MPEP.
Allosteric potentiation of mGluR1 ameliorated dentate gyrus LTP and gamma suppression.
CA3-lesioning prevented MPEP-induced CA1-LTP enhancement, indicating dentate gyrus dependency.

Conclusions:

Prolonged mGluR5 inactivation alters hippocampal LTP and network activity, partly via impaired mGluR1 expression in the dentate gyrus.
These alterations in synaptic plasticity and network function ultimately lead to impaired long-term spatial memory.
mGluR5 plays a critical role in maintaining normal hippocampal function and spatial learning.