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Related Concept Videos

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.
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...
Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

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...

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Related Experiment Video

Updated: May 16, 2026

Ex Vivo Release of Calcitonin Gene-Related Peptide from the Trigeminovascular System in Rodents
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Calcium channels and migraine.

Daniela Pietrobon1

  • 1Dept. of Biomedical Sciences, University of Padova, Italy. daniela.pietrobon@unipd.it

Biochimica Et Biophysica Acta
|November 21, 2012
PubMed
Summary

Familial hemiplegic migraine type 1 (FHM1) is caused by mutations in the CACNA1A gene, affecting Ca(V)2.1 calcium channels. Studying these mutations in mice reveals insights into migraine mechanisms.

Area of Science:

  • Neuroscience
  • Genetics
  • Pharmacology

Background:

  • Missense mutations in the CACNA1A gene are linked to familial hemiplegic migraine type 1 (FHM1).
  • Ca(V)2.1 (P/Q-type) calcium channels are crucial for neuronal function and implicated in migraine pathogenesis.
  • Migraine is a disabling neurological disorder characterized by headache and aura.

Purpose of the Study:

  • To review the pathophysiological mechanisms of migraine headache and aura.
  • To describe the function and localization of neuronal Ca(V)2.1 channels in migraine-related brain regions.
  • To discuss the functional consequences of FHM1 mutations on Ca(V)2.1 channels and neurophysiological processes.

Main Methods:

  • Review of existing literature on FHM1, CACNA1A gene, and Ca(V)2.1 channels.

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  • Analysis of biophysical properties of recombinant and native Ca(V)2.1 channels with FHM1 mutations.
  • Investigation of neurophysiological processes in knockin mouse models carrying FHM1 mutations.

    • Main Results:

    • FHM1 mutations alter the biophysical properties of Ca(V)2.1 channels.
    • Mutations impact neurophysiological processes in the cerebral cortex and trigeminovascular system.
    • Knockin mouse models carrying FHM1 mutations provide insights into migraine pathophysiology.

    Conclusions:

    • CACNA1A mutations leading to altered Ca(V)2.1 channel function are central to FHM1.
    • Understanding these channelopathies enhances knowledge of migraine mechanisms.
    • Ca(V)2.1 channels represent a potential therapeutic target for migraine treatment.