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

12.5K
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...
12.5K
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

5.1K
5.1K
Non-gated Ion Channels01:24

Non-gated Ion Channels

8.7K
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....
8.7K
Non-gated Ion Channels01:24

Non-gated Ion Channels

4.4K
4.4K
Ion Channels01:19

Ion Channels

92.5K
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...
92.5K
Resting Potential Decay01:15

Resting Potential Decay

6.7K
The resting membrane potential of a neuron (-70mV) is sustained due to the selective ion permeability of the membrane. At the resting potential, the membrane is slightly permeable to ions like sodium (Na+) and chloride (Cl−) and highly permeable to potassium ions (K+). Differences in the ions' concentration inside the cell compared to the outside are maintained by membrane transport proteins like channels and pumps.
At rest, the K+ is the main ion that moves across the membrane...
6.7K

You might also read

Related Articles

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

Sort by
Same author

Some Like it Hot: Efficiency of the Type III Secretion System has Multiple Thermosensitive Behaviours in the Pseudomonas syringae Complex.

Molecular plant pathology·2025
Same author

Co-pyrolysis of chicken feathers and macadamia nut shells, a promising strategy to create nitrogen-enriched electrode materials for supercapacitor applications.

Bioresource technology·2024
Same author

Computing Geographical Networks Generated by Air-Mass Movement.

GeoHealth·2023
Same author

Gait characteristics during inadvertent obstacle contacts in young, middle-aged and older adults.

Gait & posture·2020
Same author

A New Semi-Selective Medium for Xanthomonas campestris pv. vitians, the Causal Agent of Bacterial Leaf Spot of Lettuce.

Plant disease·2019
Same author

Cooling reverses pathological bifurcations to spontaneous firing caused by mild traumatic injury.

Chaos (Woodbury, N.Y.)·2018
Same journal

Preface.

Current topics in membranes·2026
Same journal

Pathophysiological insights into ion channel dysregulation and electrical remodeling in cardiac cells during Trypanosoma cruzi infection.

Current topics in membranes·2026
Same journal

Thyroid hormone deficiency-induced cardiac ion channel dysfunction: Molecular mechanisms and arrhythmic implications.

Current topics in membranes·2026
Same journal

Chemically induced cardiotoxicity: Role of voltage dependent ion channels.

Current topics in membranes·2026
Same journal

ATP-sensitive potassium channels in neurons: Roles in and beyond metabolic control.

Current topics in membranes·2026
Same journal

Preface.

Current topics in membranes·2025
See all related articles

Related Experiment Video

Updated: Mar 15, 2026

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds
18:25

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds

Published on: August 25, 2013

12.1K

Nav Channels in Damaged Membranes.

C E Morris1, B Joos2

  • 1Ottawa Hospital Research Institute, Ottawa, ON, Canada.

Current Topics in Membranes
|September 3, 2016
PubMed
Summary
This summary is machine-generated.

Sick excitable cells develop "leaky" sodium channels due to membrane damage, leading to excitotoxicity. This "coupled left shift" phenomenon explains various cell dysfunctions and suggests targeted inhibitor strategies.

Keywords:
Acquired sodium channelopathyBlebExcitotoxicityHyperpolarizing shiftInflammationIschemiaMechanosensitivityMembrane damageSick excitable cellsTrauma

More Related Videos

Cell Membrane Repair Assay Using a Two-photon Laser Microscope
06:35

Cell Membrane Repair Assay Using a Two-photon Laser Microscope

Published on: January 2, 2018

13.6K
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

16.1K

Related Experiment Videos

Last Updated: Mar 15, 2026

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds
18:25

Live Imaging Assay for Assessing the Roles of Ca2+ and Sphingomyelinase in the Repair of Pore-forming Toxin Wounds

Published on: August 25, 2013

12.1K
Cell Membrane Repair Assay Using a Two-photon Laser Microscope
06:35

Cell Membrane Repair Assay Using a Two-photon Laser Microscope

Published on: January 2, 2018

13.6K
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

16.1K

Area of Science:

  • Neuroscience
  • Cell Biology
  • Biophysics

Background:

  • Sick excitable cells, injured by trauma or ischemia, exhibit acquired sodium channelopathies.
  • These channelopathies are linked to bleb-damaged membranes, causing "leaky" Nav channels.
  • This Nav channel leak exacerbates cellular damage in an excitotoxic cycle.

Purpose of the Study:

  • To explain the mechanism of acquired sodium channelopathies in injured excitable cells.
  • To introduce and define the concept of coupled left shift (CLS) in Nav channel function.
  • To demonstrate how CLS predicts diverse "sick excitable cell" phenomena.

Main Methods:

  • Analysis of the kinetic coupling between Nav channel activation and inactivation.
  • Modeling of cellular excitability incorporating Nav channel properties and membrane damage.
  • Discussion of experimental approaches, such as sawtooth ramp clamp, to test for Nav-CLS.

Main Results:

  • Bleb-induced membrane damage causes a hyperpolarizing shift in Nav channel gating (CLS).
  • CLS magnitude correlates with the intensity of cellular damage.
  • Nav-CLS modeling successfully predicts phenomena ranging from hyperexcitability to depolarizing block and burst firing.

Conclusions:

  • The inherent mechanosensitivity of Nav channel activation underlies CLS.
  • Nav-CLS is a sufficient mechanism to explain the dysfunction of sick excitable cells.
  • Targeting bleb-damaged membranes with smart Nav inhibitors could offer therapeutic benefits.