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

Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

3.1K
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...
3.1K
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

9.2K
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...
9.2K
Ligand-gated Ion Channels01:19

Ligand-gated Ion Channels

13.2K
Ligand-gated ion channels are transmembrane proteins with a channel for ions to pass through and a binding site for a ligand. The channel opens only when a ligand attaches to the binding site.
Three Subfamilies of Ligand-gated Ion Channels
Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that...
13.2K
Chemical Synapses01:26

Chemical Synapses

10.0K
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...
10.0K
Chemical Synapses01:26

Chemical Synapses

3.6K
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...
3.6K

You might also read

Related Articles

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

Sort by
Same author

Nonspecific block of voltage-gated potassium channels has greater effect on distal schaffer collaterals than proximal schaffer collaterals during periods of high activity.

Physiological reports·2017
See all related articles

Related Experiment Video

Updated: Oct 25, 2025

Preparation of Acute Spinal Cord Slices for Whole-cell Patch-clamp Recording in Substantia Gelatinosa Neurons
08:30

Preparation of Acute Spinal Cord Slices for Whole-cell Patch-clamp Recording in Substantia Gelatinosa Neurons

Published on: January 18, 2019

14.5K

Effects of divalent cations on Schaffer collateral axon function.

Benjamin Owen1,2, Franklin Woode3,4, Lawrence M Grover3

  • 1Department of Pharmacology/Physiology/Toxicology, Marshall University, Huntington, WV, 25755, USA. benjamin.owen@vumc.org.

Experimental Brain Research
|August 7, 2021
PubMed
Summary

Altering extracellular calcium and magnesium levels affects neuronal excitability changes during high-frequency stimulation (HFS). Changes in calcium influenced early hyper-excitability, while magnesium affected later depression.

Keywords:
CA1CalciumHippocampusHyper-excitabilityMagnesium

More Related Videos

Acute Dissociation of Lamprey Reticulospinal Axons to Enable Recording from the Release Face Membrane of Individual Functional Presynaptic Terminals
12:01

Acute Dissociation of Lamprey Reticulospinal Axons to Enable Recording from the Release Face Membrane of Individual Functional Presynaptic Terminals

Published on: October 1, 2014

9.0K
Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

9.1K

Related Experiment Videos

Last Updated: Oct 25, 2025

Preparation of Acute Spinal Cord Slices for Whole-cell Patch-clamp Recording in Substantia Gelatinosa Neurons
08:30

Preparation of Acute Spinal Cord Slices for Whole-cell Patch-clamp Recording in Substantia Gelatinosa Neurons

Published on: January 18, 2019

14.5K
Acute Dissociation of Lamprey Reticulospinal Axons to Enable Recording from the Release Face Membrane of Individual Functional Presynaptic Terminals
12:01

Acute Dissociation of Lamprey Reticulospinal Axons to Enable Recording from the Release Face Membrane of Individual Functional Presynaptic Terminals

Published on: October 1, 2014

9.0K
Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure
09:34

Use of In Vivo Single-fiber Recording and Intact Dorsal Root Ganglion with Attached Sciatic Nerve to Examine the Mechanism of Conduction Failure

Published on: August 27, 2019

9.1K

Area of Science:

  • Neuroscience
  • Neurophysiology

Background:

  • Distal Schaffer collaterals exhibit biphasic excitability changes (hyper-excitability followed by depression) during high-frequency stimulation (HFS).
  • Extracellular divalent cations, calcium (Ca2+) and magnesium (Mg2+), are known modulators of neuronal membrane excitability.

Purpose of the Study:

  • To investigate the hypothesis that altering extracellular Ca2+ and Mg2+ concentrations modifies the biphasic excitability changes in hippocampal CA1 Schaffer collaterals during HFS.
  • To elucidate the role of divalent cations in regulating neuronal excitability patterns.

Main Methods:

  • Electrophysiological recordings of distal Schaffer collateral fiber volleys in hippocampal area CA1 during 100 Hz HFS.
  • Utilized artificial cerebrospinal fluid (ACSF) with varied concentrations of Ca2+ and Mg2+ (normal, high Ca2+/low Mg2+, low Ca2+/high Mg2+, high Ca2+/normal Mg2+, normal Ca2+/high Mg2+).
  • Tested the involvement of voltage-gated calcium channels (CaV) using specific blockers (ω-agatoxin IVA, ω-conotoxin-GVIA, cadmium).

Main Results:

  • Increased extracellular Ca2+ enhanced the early hyper-excitability period, while decreased Ca2+ reduced it.
  • Increased extracellular Mg2+ attenuated the later excitability depression period.
  • Blockade of CaV channels did not affect the observed responses during HFS, suggesting Ca2+ influx through these channels is not the primary mechanism.

Conclusions:

  • Extracellular Ca2+ and Mg2+ concentrations significantly modulate the biphasic excitability dynamics of Schaffer collaterals during HFS.
  • While altered membrane surface charge may contribute, Ca2+ influx through voltage-gated channels is not essential for these observed effects.
  • These findings highlight the critical role of extracellular ion balance in regulating neuronal network activity patterns.