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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.
The Role of Ion Channels in Neuronal Computation01:19

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.
Long-term Depression01:03

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 Depression01:05

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 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...

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Related Experiment Video

Updated: May 14, 2026

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices
10:35

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices

Published on: March 15, 2018

Calcium channels and short-term synaptic plasticity.

William A Catterall1, Karina Leal, Evanthia Nanou

  • 1Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA.

The Journal of Biological Chemistry
|February 13, 2013
PubMed
Summary

Voltage-gated calcium channels (Ca(V)2.1) control neurotransmitter release. Their regulation by calcium and calmodulin significantly impacts short-term synaptic plasticity, influencing information processing in the nervous system.

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Last Updated: May 14, 2026

Two-photon Calcium Imaging in Neuronal Dendrites in Brain Slices
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Published on: March 15, 2018

Investigating Long-term Synaptic Plasticity in Interlamellar Hippocampus CA1 by Electrophysiological Field Recording
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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cellular Physiology

Background:

  • Voltage-gated calcium channels initiate neurotransmitter release at presynaptic nerve terminals.
  • Synaptic transmission strength is highly sensitive to calcium influx.
  • Short-term synaptic plasticity (milliseconds) is crucial for neural information encoding.

Purpose of the Study:

  • To review the role of Ca(V)2.1 channel regulation in short-term synaptic plasticity.
  • To highlight the contribution of Ca(2+)-dependent mechanisms to synaptic diversity.

Main Methods:

  • Literature review of studies on voltage-gated calcium channels.
  • Analysis of Ca(2+)-calmodulin interactions with Ca(V)2.1 channels.
  • Examination of evidence linking channel regulation to synaptic plasticity.

Main Results:

  • Ca(V)2.1 channels are the primary calcium source for CNS neurotransmission.
  • Calcium and calmodulin tightly regulate Ca(V)2.1 channel activity, causing facilitation and inactivation.
  • This regulation is a key mechanism underlying short-term synaptic plasticity.

Conclusions:

  • Regulation of Ca(V)2.1 channels by calcium-sensing proteins is a major driver of short-term synaptic plasticity.
  • Understanding these mechanisms is vital for comprehending synaptic strength modulation and information processing in the brain.