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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.

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...

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...

Postsynaptic Potential (PSP)

Postsynaptic Potential (PSP)

Postsynaptic potential (PSP) refers to a change in the electrical potential of a neuron when neurotransmitters released by presynaptic neurons bind to postsynaptic receptors. This potential can either be excitatory, leading to depolarization and ultimately action potential generation, or inhibitory, leading to hyperpolarization and suppression of the postsynaptic neuron.
There are two types of receptors: ionotropic and metabotropic.
The ionotropic receptor is the membrane protein that has an...

Integration of Synaptic Events

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...

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Related Experiment Video

Updated: Jun 10, 2026

3D Modeling of Dendritic Spines with Synaptic Plasticity

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Active zone plasticity couples sleep need to presynaptic hypophosphorylation.

Chengji Piao^1,2, Ewelina P Dutkiewicz³, Laxmikanth Kollipara³

¹Institute for Biology/Genetics, Freie Universität Berlin, Berlin 14195, Germany.

Proceedings of the National Academy of Sciences of the United States of America

|June 8, 2026

Summary

Sleep loss in fruit flies alters presynaptic protein phosphorylation, reducing sleep need. This hypophosphorylation, linked to specific enzymes, suggests a conserved mechanism for synaptic adaptation to sleep debt.

Keywords:

Bruchpilot (BRP)active zone phosphorylation sleep homeostasis synaptic plasticity

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Last Updated: Jun 10, 2026

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Published on: May 18, 2020

The Sleep Nullifying Apparatus: A Highly Efficient Method of Sleep Depriving Drosophila

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Published on: December 14, 2020

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Published on: September 4, 2015

Area of Science:

Neuroscience
Molecular Biology
Sleep Research

Background:

Sleep homeostasis involves synaptic plasticity, but specific molecular changes are unclear.
In Drosophila, sleep loss increases Bruchpilot (BRP) at presynaptic active zones.
Previous work established BRP gene dosage as a modulator of sleep pressure.

Purpose of the Study:

To investigate the molecular mechanisms of sleep-dependent synaptic plasticity.
To identify changes in protein phosphorylation and other pathways in response to sleep loss.

Main Methods:

Synapse-enriched integrated-omics (proteomics, phospho-proteomics) in Drosophila.
Bioinformatic analysis of proteomic data.
Genetic manipulation of kinase and phosphatase activity (PKA, PP1).

Main Results:

Sleep loss induced changes in immune/stress response pathways and local translation.
A global shift towards presynaptic protein hypophosphorylation was observed.
Reduced Protein Kinase A (PKA) activity and enhanced Protein Phosphatase 1 (PP1) activity likely mediate hypophosphorylation.
Manipulating PKA or PP1 reversed BRP-modulated sleep phenotypes.

Conclusions:

Presynaptic hypophosphorylation is a molecular signature of synaptic remodeling during sleep need.
This adaptive tuning of sleep need involves reversible posttranslational modifications.
The identified mechanism is potentially conserved across species.