Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Antiepileptic Drugs: Modulators of Neurotransmitter Release Mediated by SV2A Protein

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...

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

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...

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...

Voltage-gated Ion Channels

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...

Excitatory and Inhibitory Effects of Neurotransmitters

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of...

Chemical Synapses

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...

You might also read

Related Articles

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

Sort by

Same author

New onset refractory status epilepticus (NORSE) versus refractory status epilepticus not meeting NORSE criteria: A comparative clinical and electroencephalography-based study.

Epilepsia·2026

Same author

Next-generation chemogenetic inhibition using a brain-permeant non-prescription agent.

Signal transduction and targeted therapy·2026

Same author

UCL Queen Square Institute of Neurology: 75 years of innovation.

The Lancet. Neurology·2026

Same author

Effective communication in the pharmacy.

Ceska a Slovenska farmacie : casopis Ceske farmaceuticke spolecnosti a Slovenske farmaceuticke spolecnosti·2026

Same author

Anhedonic Traits Do Not Impair Performance in a 3-Arm Bandit Task.

Computational psychiatry (Cambridge, Mass.)·2026

Same author

The Extremely Brilliant Brain: An Isotropic Microscale Human Brain Dataset.

bioRxiv : the preprint server for biology·2026

Search research articles

Related Experiment Video

Updated: Mar 7, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Published on: April 23, 2019

Kv1.1 channelopathy abolishes presynaptic spike width modulation by subthreshold somatic depolarization.

Umesh Vivekananda¹, Pavel Novak², Oscar D Bello¹

¹Institute of Neurology, University College London, London WC1N 3BG, United Kingdom.

Proceedings of the National Academy of Sciences of the United States of America

|February 15, 2017

Summary

Subthreshold membrane potential fluctuations influence neurotransmitter release by altering action potential width. The Kv1.1 potassium channel subunit is not essential for this modulation, but a disease-associated mutation disrupts it.

Keywords:

channelopathy potassium channel synaptic transmission

More Related Videos

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

Profiling Voltage-gated Potassium Channel mRNA Expression in Nigral Neurons using Single-cell RT-PCR Techniques

Profiling Voltage-gated Potassium Channel mRNA Expression in Nigral Neurons using Single-cell RT-PCR Techniques

Published on: September 27, 2011

Related Experiment Videos

Last Updated: Mar 7, 2026

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Evaluation of Synaptic Multiplicity Using Whole-cell Patch-clamp Electrophysiology

Published on: April 23, 2019

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

Profiling Voltage-gated Potassium Channel mRNA Expression in Nigral Neurons using Single-cell RT-PCR Techniques

Profiling Voltage-gated Potassium Channel mRNA Expression in Nigral Neurons using Single-cell RT-PCR Techniques

Published on: September 27, 2011

Area of Science:

Neuroscience
Cellular Biology
Biophysics

Background:

Action potentials are typically all-or-none, but subthreshold somatic potentials can modulate synaptic release.
Presynaptic Kv1-family potassium channel inactivation is a key mechanism for analog-digital modulation of action potentials.
Previous studies using axon transections may not accurately reflect in vivo conditions.

Purpose of the Study:

To investigate the role of distinct potassium channels in basal presynaptic action potential width.
To determine how subthreshold somatic depolarization modulates action potential width in intact synaptic boutons.
To elucidate the interaction between Kv1.1 channels and spike modulation.

Main Methods:

Recordings from small boutons in primary hippocampal cultures using intact axons.
Identification of boutons with scanning ion conductance microscopy.
Pharmacological and genetic manipulation of Kv1.1 potassium channels, including a heterozygous mouse model of episodic ataxia type 1.

Main Results:

Deletion of Kv1.1 broadened presynaptic spikes but did not abolish modulation by somatic depolarization.
A dominant Kv1.1 mutation broadened basal spike width but abolished modulation by somatic prepulses.
These findings suggest Kv1.1 is not necessary for subthreshold modulation of spike width.

Conclusions:

The Kv1.1 subunit is not essential for subthreshold modulation of presynaptic action potential width.
A disease-associated Kv1.1 mutation disrupts the analog-digital interplay in synaptic transmission.
This disruption may stem from altered presynaptic potassium channel stoichiometry.