Related Experiment Video
Updated: Jul 4, 2026
11:08
Double-barreled and Concentric Microelectrodes for Measurement of Extracellular Ion Signals in Brain Tissue
Published on: September 5, 2015
GluR6/KA2 kainate receptors mediate slow-deactivating currents
Andrea Barberis1, Shankar Sachidhanandam, Christophe Mulle
1Laboratoire Physiologie Cellulaire de la Synapse, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5091, Bordeaux Neuroscience Institute, University of Bordeaux 2, 33077 Bordeaux, France. andrea.barberis@iit.it
Summary
Synaptic kainate receptors (KARs) exhibit slow signaling, unlike their fast-acting recombinant counterparts. This study reveals GluR6/KA2 receptor gating explains the slow decay of kainate receptor-EPSCs, crucial for synaptic integration.
Area of Science:
- Neuroscience
- Molecular Biology
- Biophysics
Background:
- Kainate receptors (KARs) are ionotropic glutamate receptors vital for synaptic transmission.
- Synaptic KARs mediate slow excitatory postsynaptic currents (EPSCs), essential for neural integration.
- Recombinant KARs in heterologous systems display faster kinetics than synaptic KARs, a discrepancy lacking explanation.
Purpose of the Study:
- Investigate the properties of recombinant heteromeric GluR6/KA2 receptors, which form synaptic KARs.
- Explain the slow decay kinetics observed in synaptic KAR-EPSCs.
- Determine the molecular mechanisms underlying KAR-EPSC kinetics.
Main Methods:
- Studied recombinant heteromeric GluR6/KA2 receptors.
- Applied brief glutamate applications to receptor systems.
- Utilized computational modeling and simulations.
- Analyzed receptor gating and current decay properties.
Main Results:
- Recombinant GluR6/KA2 receptors, unlike GluR6 receptors, exhibited slow current decay upon brief glutamate exposure.
- The decay time course of GluR6/KA2 currents mimicked synaptic KAR-EPSCs.
- Model simulations indicated slow deactivation due to stabilized partially bound open states in GluR6/KA2 receptors.
Conclusions:
- The gating properties of GluR6/KA2 receptors likely contribute to the slow decay kinetics of synaptic KAR-EPSCs.
- This finding resolves the kinetic discrepancy between synaptic and recombinant KARs.
- Highlights the importance of receptor subunit composition in determining channel kinetics and synaptic function.
More Related Videos
Related Concept Videos
01:30Ligand-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...
01:21G-Protein Gated Ion Channels
GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Sensory organs,...
01:28Depolarizing Blockers: Mechanism of Action
Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
01:19The 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.
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.
01:12GPCR Desensitization
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
01:24Non-gated Ion Channels
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.
Compared to the gated ion channels, the non-gated channels, also known as leakage or passive channels, have no gating mechanism.