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

Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
Non-gated Ion Channels01:24

Non-gated Ion Channels

Ion channels are specialized proteins on the plasma membrane that allow charged ions to pass down their electrochemical gradient. Their main function is to maintain the membrane potential which is critical for cell viability. These channels are either gated or non-gated and can transport more than a thousand ions within milliseconds for the cellular event to occur.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.
Ion Channels01:19

Ion Channels

The movement of ions like sodium, potassium, and calcium into and out of the cell is essential to maintain the electrochemical gradient in living cells. The ion channels—a class of membrane transport proteins—help maintain this ionic gradient for the smooth functioning of physiological activities such as maintaining cell size and volume, conducting nerve impulses, and gas and nutrient exchange.
Ion channels are specialized integral membrane proteins on the plasma membrane that allow specific...
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.

You might also read

Related Articles

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

Sort by
Same author

Naturally occurring ACE2 stalk variants are differentially released from the cell.

Scientific reports·2026
Same author

Salmonella SopB suppresses post-transcriptionally regulated cytokine release to reduce early tissue inflammation and delay disease progression.

Nature communications·2026
Same author

Transferrin receptor 1 shedding by the pro-inflammatory iRhom-ADAM17 complex and ADAM10 regulates cellular iron uptake and ferroptosis.

Experimental & molecular medicine·2026
Same author

Naturally occurring ACE2 stalk variants are differentially released from the cell.

bioRxiv : the preprint server for biology·2026
Same author

Modelling inflammatory endothelial dysfunction: a human in vitro platform for translational research.

Frontiers in bioengineering and biotechnology·2026
Same author

ADAM10 and ADAM17 differently mediate induced pulmonary ACE release by either direct proteolysis or indirect upregulation protein synthesis.

Biochimica et biophysica acta. Molecular cell research·2026

Related Experiment Video

Updated: Jul 14, 2026

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
10:20

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b

Published on: November 11, 2016

Pathophysiology of HCN channels.

Stefan Herrmann1, Juliane Stieber, Andreas Ludwig

  • 1Institut für Experimentelle und Klinische Pharmakologie und Toxikologie, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.

Pflugers Archiv : European Journal of Physiology
|June 6, 2007
PubMed
Summary

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are crucial for neuron and cardiac function. Gene-deficient mice reveal distinct roles for HCN1-4 in learning, epilepsy, and heart development.

More Related Videos

Recapitulation of an Ion Channel IV Curve Using Frequency Components
10:14

Recapitulation of an Ion Channel IV Curve Using Frequency Components

Published on: February 8, 2011

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane
07:38

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane

Published on: March 30, 2015

Related Experiment Videos

Last Updated: Jul 14, 2026

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
10:20

Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b

Published on: November 11, 2016

Recapitulation of an Ion Channel IV Curve Using Frequency Components
10:14

Recapitulation of an Ion Channel IV Curve Using Frequency Components

Published on: February 8, 2011

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane
07:38

Functional Characterization of Na+/H+ Exchangers of Intracellular Compartments Using Proton-killing Selection to Express Them at the Plasma Membrane

Published on: March 30, 2015

Area of Science:

  • Neuroscience
  • Cardiology
  • Molecular Biology

Background:

  • Hyperpolarization-activated cation currents (I(f/h)) are vital in neurons and cardiac cells.
  • Four genes (HCN1-4) encode the channels responsible for these currents.
  • Understanding HCN channel function is key to neurological and cardiac health.

Purpose of the Study:

  • To review the physiology and pathophysiology of HCN channel family members.
  • To highlight insights gained from HCN gene-deficient mouse models.
  • To correlate findings with human HCN4 channel defects.

Main Methods:

  • Analysis of transgenic mouse models with specific HCN gene deletions (HCN1, HCN2, HCN4).
  • Phenotypic characterization of motor learning, spatial memory, epilepsy, ataxia, and cardiac function.
  • Review of data from human patients with HCN4 channel defects.

Main Results:

  • HCN1 deficiency impairs motor learning but enhances spatial memory.
  • HCN2 deletion leads to absence epilepsy, ataxia, and sinus node dysfunction.
  • HCN4 null mice exhibit embryonic lethality and lack sinoatrial node activity.

Conclusions:

  • Distinct HCN subunits (HCN1-4) have unique and critical roles in the nervous and cardiac systems.
  • Transgenic mouse models provide essential insights into HCN channel pathophysiology.
  • HCN channel dysfunction underlies significant human diseases, including epilepsy and cardiac arrhythmias.