Calcium channel antagonist omega-conotoxin binds to intramembrane particles of isolated nerve terminals

I Fariñas1, G Egea, J Blasi

  • 1Departament de Biologia Cellular i Anatomia Patològica, Facultat de Medicina, Hospital de Bellvitge, Universitat de Barcelona, Spain.

Neuroscience
|June 1, 1993
PubMed

Insights

Voltage-sensitive calcium channels are crucial for neurotransmitter release. This study identifies these channels as intramembrane particles in presynaptic membranes using a specific toxin, confirming their role in fast synaptic signaling.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Voltage-sensitive calcium channels are vital for neurotransmitter release at chemical synapses.
  • Their precise localization in presynaptic membranes is essential for rapid synaptic transmission.

Purpose of the Study:

  • To identify and localize voltage-sensitive calcium channels in presynaptic membranes.
  • To confirm the role of intramembrane particles as calcium channels.

Main Methods:

  • Utilized a biotinylated omega-conotoxin, a neuronal calcium channel antagonist.
  • Employed colloidal gold labeling and freeze-fracture techniques for visualization.
  • Isolated nerve terminals from the electric organ of Torpedo marmorata.

Main Results:

  • The biotinylated omega-conotoxin specifically bound to intramembrane particles in presynaptic membranes.
  • This binding inhibited high potassium-evoked adenosine triphosphate release, similar to the native toxin.
  • Displacement experiments confirmed the specific interaction of the blocker with biological membranes.

Conclusions:

  • Intramembrane particles concentrated at neurotransmitter release sites represent voltage-activated calcium channels.
  • This finding reinforces the structural and functional understanding of fast synaptic signaling.
  • Provides direct evidence linking specific membrane structures to calcium channel function.

Related Concept Videos

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...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin01:26

Directly Acting Muscle Relaxants: Dantrolene and Botulinum Toxin

Directly acting muscle relaxants like dantrolene and botulinum toxin (BoNT) have distinct mechanisms and applications. Dantrolene, a hydantoin derivative, acts on the ryanodine receptor (RYR1) in skeletal muscle cells. RYR1 are calcium channels present at the sarcoplasmic reticulum membrane. In response to excitation, they release calcium ions from the sarcoplasmic reticulum to the cytosol. Calcium promotes actin-myosin-mediated contraction of muscles.
The binding of dantrolene to the RYR1...
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,...