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Related Concept Videos

Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
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.
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 24, 2026

Pull-down of Calmodulin-binding Proteins
07:51

Pull-down of Calmodulin-binding Proteins

Published on: January 23, 2012

Ca/Calmodulin and presynaptic short-term plasticity.

Sumiko Mochida1

  • 1Department of Physiology, Tokyo Medical University, 1-1 Shinjuku-6-chome, Shinjuku-ku, Tokyo 160-8402, Japan.

ISRN Neurology
|March 6, 2012
PubMed
Summary
This summary is machine-generated.

Neuronal firing regulates synaptic strength by controlling presynaptic calcium (Ca2+) influx and release. Ca2+-binding proteins like calmodulin modulate synaptic plasticity and neurotransmitter release.

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Pull-down of Calmodulin-binding Proteins
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Published on: January 23, 2012

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation
09:39

Improved Preparation and Preservation of Hippocampal Mouse Slices for a Very Stable and Reproducible Recording of Long-term Potentiation

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3D Modeling of Dendritic Spines with Synaptic Plasticity
07:13

3D Modeling of Dendritic Spines with Synaptic Plasticity

Published on: May 18, 2020

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Synaptic efficacy is dynamically regulated by neuronal activity at the presynaptic terminal.
  • Presynaptic activity influences transmitter release, leading to postsynaptic plasticity.
  • Calcium ions (Ca2+) are critical regulators of neurotransmitter release, entering via voltage-gated Ca2+ (CaV) channels.

Purpose of the Study:

  • To elucidate the role of Ca2+ and Ca2+-binding proteins in presynaptic plasticity.
  • To understand how Ca2+ dynamics influence synaptic facilitation and depression.
  • To investigate the interaction of calmodulin with CaV2 channels and autoreceptors in exocytosis.

Main Methods:

  • Analysis of presynaptic Ca2+ dynamics during neuronal firing.
  • Investigating the function of Ca2+-binding proteins in regulating CaV channel gating.
  • Studying the modulation of SNARE-mediated exocytosis by calmodulin.

Main Results:

  • Presynaptic Ca2+ influx through CaV channels triggers and regulates neurotransmitter release.
  • Residual Ca2+ is sensed by Ca2+-binding proteins, influencing synaptic plasticity.
  • Calmodulin interacts with CaV2 channels and autoreceptors to modulate exocytosis.

Conclusions:

  • Neuronal firing-dependent Ca2+ signaling is a key mechanism for synaptic plasticity.
  • Ca2+-binding proteins play crucial roles in mediating short-term synaptic plasticity.
  • Calmodulin is a significant modulator of presynaptic transmitter release and synaptic efficacy.