Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The Role of Ion Channels in Neuronal Computation01:19

The Role of Ion Channels in Neuronal Computation

3.2K
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....
3.2K
Chemical Synapses01:26

Chemical Synapses

9.4K
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...
9.4K
Feedback Regulation of Calcium Concentration01:27

Feedback Regulation of Calcium Concentration

2.9K
Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
2.9K
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

4.9K
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,...
4.9K
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

4.6K
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...
4.6K
Chemical Synapses01:26

Chemical Synapses

10.8K
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...
10.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[Clinical challenges and research progress in variants of uncertain significance of inherited cardiovascular diseases].

Zhonghua xin xue guan bing za zhi·2026
Same author

[Essentials and considerations for outpatient genetic counseling for inherited cardiovascular diseases].

Zhonghua xin xue guan bing za zhi·2026
Same author

[Distribution characteristics of PKP2 non-synonymous variations in protein domain and genotype-phenotype relationship in patients with arrhythmogenic right ventricular cardiomyopathy].

Zhonghua xin xue guan bing za zhi·2026
Same author

Intermediate-term risk of cardiac allograft vasculopathy following heart transplantation from hepatitis C viremic donors in the era of direct-acting antiviral therapy.

JHLT open·2025
Same author

[Sperm donation utilization rates in nonobstructive azoospermia patients under different testicular sperm retrieval methods during assisted reproductive technology cycles].

Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences·2025
Same author

[Electrocardiographic characteristics of cardiomyopathy].

Zhonghua xin xue guan bing za zhi·2025

Related Experiment Video

Updated: Apr 29, 2026

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals
08:38

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals

Published on: May 25, 2011

17.2K

Calcium stores regulate the polarity and input specificity of synaptic modification.

M Nishiyama1, K Hong, K Mikoshiba

  • 1Department of Biology, University of California at San Diego, La Jolla 92093-0357, USA.

Nature
|December 16, 2000
PubMed
Summary

Activity-induced synaptic plasticity, like long-term potentiation (LTP) or depression (LTD), depends on postsynaptic calcium. Calcium influx and release from internal stores regulate synaptic modification polarity and specificity.

More Related Videos

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

11.0K
Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
09:07

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis

Published on: February 18, 2020

9.4K

Related Experiment Videos

Last Updated: Apr 29, 2026

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals
08:38

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals

Published on: May 25, 2011

17.2K
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

11.0K
Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
09:07

Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis

Published on: February 18, 2020

9.4K

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Molecular Biology

Background:

  • Synaptic modification, including long-term potentiation (LTP) and long-term depression (LTD), is crucial for nervous system development and plasticity.
  • Activity-dependent changes in synaptic efficacy are fundamental to learning and memory.
  • A key question is whether these modifications are confined to activated synapses.

Purpose of the Study:

  • To investigate the role of postsynaptic calcium influx and internal calcium stores in regulating synaptic plasticity.
  • To determine the input specificity of long-term potentiation (LTP) and long-term depression (LTD) induction.
  • To elucidate the mechanisms underlying the polarity and specificity of activity-induced synaptic modifications.

Main Methods:

  • Electrophysiological recordings in the CA1 region of the hippocampus.
  • Pharmacological blockade of NMDA (N-methyl-D-aspartate) receptors to modulate postsynaptic calcium influx.
  • Inhibition of ryanodine receptors and inositol triphosphate (InsP3) receptors to study intracellular calcium release.
  • Genetic deletion of type 1 InsP3 receptors.

Main Results:

  • Partial blockade of NMDA receptors converted LTP to LTD and induced LTD at heterosynaptic inputs.
  • Induction of homosynaptic LTD required functional ryanodine receptors, while heterosynaptic LTD required InsP3 receptors.
  • Blocking ryanodine receptors abolished homosynaptic LTD but not heterosynaptic LTD.
  • Genetic deletion of type 1 InsP3 receptors converted LTD to LTP and eliminated heterosynaptic LTD.

Conclusions:

  • Postsynaptic calcium, influenced by influx and release from ryanodine and InsP3 receptors, dictates both the direction (LTP/LTD) and specificity of synaptic modifications.
  • Differential activation of intracellular calcium stores plays a critical role in determining homosynaptic versus heterosynaptic plasticity.
  • These findings reveal a sophisticated mechanism controlling synaptic plasticity based on calcium dynamics.