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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.

The Role of Ion Channels in Neuronal Computation

The Role of Ion Channels in Neuronal Computation

A postsynaptic neuron usually receives numerous impulses from several other presynaptic neurons. The axon hillock of the postsynaptic neuron integrates all these signals and determines the likelihood of firing an action potential.
Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron. However, multiple presynaptic inputs must often create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.

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...

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...

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Related Experiment Video

Updated: Jun 18, 2026

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Published on: March 15, 2018

Neuronal calcium sensors and synaptic plasticity.

Mascia Amici¹, Andrew Doherty, Jihoon Jo

¹Department of Anatomy, MRC Centre for Synaptic Plasticity, University of Bristol, Bristol, UK. Mascia.Amici@bristol.ac.uk

Biochemical Society Transactions

|November 14, 2009

Summary

Neuronal calcium sensor (NCS) proteins, including NCS-1 and hippocalcin, are crucial for synaptic plasticity. This review highlights their emerging roles in regulating long-term potentiation (LTP) and long-term depression (LTD) signaling pathways.

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Published on: July 15, 2012

Area of Science:

Neuroscience
Molecular Biology
Cell Signaling

Background:

Calcium entry is critical for synaptic plasticity, influencing long-term potentiation (LTP) and long-term depression (LTD).
The precise molecular mechanisms underlying synaptic plasticity induction remain incompletely understood.
Calcium sensor proteins are key regulators of initial signaling events in synaptic plasticity.

Purpose of the Study:

To review and synthesize current evidence on the role of neuronal calcium sensor (NCS) proteins in synaptic plasticity.
To highlight the emerging functions of NCS-1 and hippocalcin in this process.

Main Methods:

Literature review and synthesis of existing research findings.
Focus on studies investigating NCS protein involvement in central nervous system plasticity.

Main Results:

NCS proteins play a significant role in the spatiotemporal regulation of calcium signals that determine synaptic plasticity outcomes.
Emerging evidence implicates NCS-1 and hippocalcin as important mediators in LTP and LTD pathways.

Conclusions:

NCS proteins are essential components of synaptic plasticity signaling cascades.
Further research into NCS-1 and hippocalcin will elucidate critical aspects of neuronal function and plasticity.