Related Experiment Video

Updated: Aug 8, 2026

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals
08:38

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals

Published on: May 25, 2011

The influence exerted by the beta(3) subunit on MVIIA omega-conotoxin binding to neuronal N-type calcium channels

T Luchian1

  • 1Faculty of Physics, Department of Biophysics and Medical Physics, 'Alexandru I. Cuza' University, Blvd. Carol I No. 11, R-6600, Iasi, Romania. luchian@uaic.ro

Biochimica Et Biophysica Acta
|June 19, 2001
PubMed

Insights

The beta(3) subunit modifies N-type calcium channel activity, impacting MVIIA omega-conotoxin binding. This interaction alters channel gating, affecting how the toxin inhibits calcium currents.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • N-type calcium channels are crucial for neurotransmitter release.
  • MVIIA omega-conotoxin is a selective blocker of N-type calcium channels.
  • Beta subunits modulate calcium channel function.

Purpose of the Study:

  • To investigate the role of the beta(3) subunit in MVIIA omega-conotoxin's interaction with the alpha(1B-d) N-type calcium channel.
  • To elucidate the molecular mechanisms underlying beta subunit modulation of toxin binding.

Main Methods:

  • Two-electrode voltage-clamp electrophysiology.
  • Expression of cloned alpha(1B-d) calcium channel subunits in Xenopus laevis oocytes.
  • Co-expression with the beta(3) subunit.

Main Results:

  • Co-expression of the beta(3) subunit significantly altered the IC(50) for MVIIA inhibition.
  • The beta(3) subunit did not affect the gating charge of channel activation.
  • Co-expression shifted channel activation to more hyperpolarized potentials by approximately 10 mV.

Conclusions:

  • MVIIA omega-conotoxin appears to alter the surface charge of N-type calcium channels.
  • Beta(3) subunit co-expression influences MVIIA binding affinity, potentially through allosteric changes.
  • The beta(3) subunit modulates N-type calcium channel gating and toxin interaction.

More Related Videos

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons12:19

Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons

Published on: June 24, 2015

Identification and Classification of Position-specific GABAA Receptor Subunit Missense Variants for Their Role In Hippocampal Pyramidal Neurons08:04

Identification and Classification of Position-specific GABAA Receptor Subunit Missense Variants for Their Role In Hippocampal Pyramidal Neurons

Published on: June 6, 2025

Related Concept Videos

G-Protein Gated Ion Channels01:21

G-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,...
Calmodulin-dependent Signaling01:16

Calmodulin-dependent Signaling

Calmodulin (CaM) is a calcium-binding protein in eukaryotes that controls various calcium-regulated cellular processes. It has four calcium-binding sites that bind calcium to form the calcium-calmodulin ( Ca2+-CaM) complex. GPCR stimulation increases the calcium levels in the cells that bind to CaM and induces a conformational change.
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
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...
Neurochemical Transmission: Sites of Drug Action01:26

Neurochemical Transmission: Sites of Drug Action

Neurochemical transmission, the conduction of electrical impulses between neurons mediated by neurotransmitters, plays a vital role in various physiological processes. Autonomic drugs exert their effects by modulating neurotransmission within the autonomic nervous system. For instance, drugs such as hemicholinium block the precursor uptake necessary for synthesizing acetylcholine, an essential autonomic neurotransmitter. Following synthesis, neurotransmitters are stored in vesicles. Metyrosine...
Cholinergic Receptors: Muscarinic01:25

Cholinergic Receptors: Muscarinic

The pharmacological actions of acetylcholine are elicited via its binding to two families of cholinergic receptors or cholinoceptors, namely, muscarinic and nicotinic receptors. Muscarinic receptors are G protein-coupled receptors and have five subtypes, M1–M5. All mAChR subtypes are activated by acetylcholine and blocked by the antagonist, atropine. 
The subtypes M1, M3, and M5 couple with the Gq subunit and activate the phospholipase C (PLC) activity, mobilizing intracellular Ca2+. Activation...
Cholinergic Receptors: Nicotinic01:15

Cholinergic Receptors: Nicotinic

Nicotinic receptors are ligand-gated ion channels that are activated by acetylcholine and nicotine. Upon activation, they cause a rapid increase in the permeability of cells to K+, Na+, and Ca2+, followed by depolarization and excitation. They are in the autonomic ganglia, skeletal neuromuscular junction, CNS, and adrenal medulla.
There are two types of nicotinic receptors: neuromuscular (NM/NM/N1) and neuronal (NN/NN/N2). The two families differ based on their location and selectivity to...