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

Epilepsy and Seizures: Overview01:24

Epilepsy and Seizures: Overview

Epilepsy is a chronic neurological disease marked by recurrent, unpredictable seizures. These seizures are caused by abnormal electrical discharges in the brain, leading to behavior, sensation, or consciousness alterations. They can also cause transient impairment of awareness, interfering with daily activities.
Various factors can trigger epilepsy, including genetic factors, brain damage, metabolic causes, and unknown etiology. Diagnosis of epilepsy involves electroencephalography (EEG), which...
Antiepileptic Drugs: Calcium Channel Blockers01:17

Antiepileptic Drugs: Calcium Channel Blockers

Calcium channel blockers, a class of antiepileptic drugs, regulate the flow of calcium ions within neurons.
Calcium channel blockers exert their antiepileptic effects by targeting T-type calcium channels, which are integral to transmitting nerve signals in the central nervous system. These channels allow the passage of calcium ions, which are vital for neuronal communication. By inhibiting T-type calcium channels, calcium channel blockers effectively reduce the release of neurotransmitters and...
Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein01:20

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

Antiepileptic drugs, such as levetiracetam (Keppra) and brivaracetam (Briviact), have emerged as crucial tools in managing epilepsy. These medications exert their therapeutic effects by targeting the synaptic vesicle protein SV2A, a transmembrane glycoprotein primarily found in the brain.
SV2A is a transmembrane glycoprotein located predominantly in the brain, modulating the release of neurotransmitters for neuronal communication. Both levetiracetam and brivaracetam exhibit a high affinity for...
Antiepileptic Drugs: Potassium Channel Activators01:20

Antiepileptic Drugs: Potassium Channel Activators

Ezocgabine or retigabine, an antiepileptic drug of remarkable efficacy, has revolutionized the management of seizures. It is a potassium channel activator, explicitly targeting the family of Q subtype potassium channels. It enhances the transmembrane potassium currents, regulating neuronal excitability. This action stabilizes the resting membrane potential, a pivotal factor in mitigating the hyperexcitability that characterizes epilepsy.
Ezogabine has gained approval as an adjunctive treatment...
Antiepileptic Drugs: Sodium Channel Blockers01:08

Antiepileptic Drugs: Sodium Channel Blockers

Antiepileptic drugs are specialized medications that prevent seizures in individuals diagnosed with epilepsy. These drugs primarily function by blocking the movement of sodium ions through channels in the neuronal membrane, inhibiting the repetitive firing of action potentials often associated with seizures.
Sodium channel blockers modulate ion channels, particularly voltage-gated sodium channels. They block only sodium ion movement.
Among the most commonly prescribed antiepileptic drugs are...
Epilepsy ll: Types01:22

Epilepsy ll: Types

Recurrent seizures, stemming from abnormal electrical activity in the brain, are the defining characteristic of epilepsy, a chronic neurological condition. Because seizure features vary greatly, epilepsy is classified using two systems: by seizure type and by epilepsy syndromes. These classifications enable clinicians to describe seizure patterns and select suitable treatment strategies.I. Classification by Seizure Type1. Focal EpilepsyFocal epilepsy begins in one hemisphere of the brain.

You might also read

Related Articles

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

Sort by
Same author

Astrocyte activation in the ventrolateral medulla modulates breathing and arousal states.

Nature communications·2026
Same author

Impact of Prior History of Traumatic Stress on Autonomic and Multi-System Symptoms Following COVID-19 Infection.

Chronic stress (Thousand Oaks, Calif.)·2025
Same author

The Concise Guide to PHARMACOLOGY 2025/26: Ion channels.

British journal of pharmacology·2025
Same author

Bottom-up design of Ca<sup>2+</sup> channels from defined selectivity filter geometry.

Nature·2025
Same author

Sleep Identification Enabled by Supervised Training Algorithms (SIESTA): An Open-Source Platform for Automatic Sleep Staging of Rodent Electrocorticographic and Electromyographic Data.

Journal of biological rhythms·2025
Same author

The role of medullary astrocytes in breathing and arousal: insights into glial regulation of respiratory function.

Research square·2025
Same journal

Diving exposure and pulmonary stress.

The Journal of physiology·2026
Same journal

Systems modelling of mitochondrial dynamics in different exercise regimes.

The Journal of physiology·2026
Same journal

Central leptin resistance precedes obesity and drives early endocrine dysfunction.

The Journal of physiology·2026
Same journal

Decoding the molecular memory of obesity using machine learning and microRNA dynamics.

The Journal of physiology·2026
Same journal

Kinematic-calcium loops unravel impaired excitation-contraction coupling in MELAS-affected cardioids.

The Journal of physiology·2026
Same journal

hERG1 channels and potential therapeutics for long QT syndrome.

The Journal of physiology·2026
See all related articles

Related Experiment Video

Updated: Jun 15, 2026

A Behavioral Screen for Heat-Induced Seizures in Mouse Models of Epilepsy
06:58

A Behavioral Screen for Heat-Induced Seizures in Mouse Models of Epilepsy

Published on: July 12, 2021

NaV1.1 channels and epilepsy.

William A Catterall1, Franck Kalume, John C Oakley

  • 1University of Washington, Department of Pharmacology, SJ-30, Seattle, WA 98195-7280, USA. wcatt@u.washington.edu

The Journal of Physiology
|March 3, 2010
PubMed
Summary
This summary is machine-generated.

Mutations in SCN1A gene

More Related Videos

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays
10:24

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Published on: May 15, 2018

In Vivo Fiber-Coupled Pre-Clinical Confocal Laser-scanning Endomicroscopy (pCLE) of Hippocampal Capillaries in Awake Mice
09:08

In Vivo Fiber-Coupled Pre-Clinical Confocal Laser-scanning Endomicroscopy (pCLE) of Hippocampal Capillaries in Awake Mice

Published on: April 21, 2023

Related Experiment Videos

Last Updated: Jun 15, 2026

A Behavioral Screen for Heat-Induced Seizures in Mouse Models of Epilepsy
06:58

A Behavioral Screen for Heat-Induced Seizures in Mouse Models of Epilepsy

Published on: July 12, 2021

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays
10:24

Recording and Modulation of Epileptiform Activity in Rodent Brain Slices Coupled to Microelectrode Arrays

Published on: May 15, 2018

In Vivo Fiber-Coupled Pre-Clinical Confocal Laser-scanning Endomicroscopy (pCLE) of Hippocampal Capillaries in Awake Mice
09:08

In Vivo Fiber-Coupled Pre-Clinical Confocal Laser-scanning Endomicroscopy (pCLE) of Hippocampal Capillaries in Awake Mice

Published on: April 21, 2023

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Voltage-gated sodium channels are crucial for action potential initiation in brain neurons.
  • Mutations in sodium channels, particularly SCN1A encoding NaV1.1, are linked to various genetic epilepsy syndromes.
  • NaV1.1 dysfunction is implicated in severe myoclonic epilepsy of infancy (SMEI/Dravet's Syndrome) and other epilepsies.

Purpose of the Study:

  • To investigate the role of NaV1.1 channel dysfunction in epilepsy.
  • To explore the spectrum of epilepsy syndromes associated with SCN1A mutations.
  • To propose a unified loss-of-function hypothesis for NaV1.1-related epilepsies.

Main Methods:

  • Analysis of loss-of-function mutations in NaV1.1 channels.
  • Electrophysiological studies in mouse models with NaV1.1 mutations.
  • Investigation of compensatory mechanisms and potential therapeutic interventions.

Main Results:

  • Loss-of-function NaV1.1 mutations impair firing in inhibitory GABAergic neurons, leading to hyperexcitability and seizures.
  • Impaired NaV1.1 function in Purkinje neurons contributes to ataxia.
  • Compensatory NaV1.6 mutations and enhanced GABAergic neurotransmission show therapeutic potential.

Conclusions:

  • A unified loss-of-function hypothesis explains the SCN1A epilepsy spectrum, from febrile seizures to SMEI.
  • NaV1.1 channel dysfunction in inhibitory neurons is a key mechanism in these epilepsy syndromes.
  • Targeting GABAergic neurotransmission offers a potential therapeutic strategy for NaV1.1-related epilepsies.