Related Experiment Video
Updated: Aug 13, 2026

Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals
Published on: May 25, 2011
Calcium-activated ATPases in presynaptic nerve endings
Calcium-activated ATPases in mouse brain synaptosomes are non-mitochondrial enzymes. These enzymes, potentially crucial for regulating intracellular calcium, show higher activity in plasma membranes and synaptic vesicles.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Presynaptic nerve endings (synaptosomes) rely on precise calcium regulation.
- Calcium-activated ATPases are key players in cellular calcium homeostasis.
Purpose of the Study:
- To investigate the properties of calcium-activated ATPases in mouse brain synaptosomes.
- To determine the localization and characteristics of these enzymes.
Main Methods:
- Isolation and subfractionation of mouse brain synaptosomes.
- Assay of ATPase activity with varying ion concentrations and substrates.
- Investigated inhibition by lanthanum (La3+) in intact and lysed synaptosomes.
Main Results:
- Synaptosomal ATPase activity was stimulated by Ca2+ and Mg2+, insensitive to Na+/K+, and hydrolyzed a high-energy phosphate bond.
- Enzymes were non-mitochondrial, inhibited by La3+ (uncompetitively in intact synaptosomes, more so after lysis).
- Ca2+-ATPase activity was higher in synaptosomal plasma membranes and synaptic vesicles, activated by physiological intracellular Ca2+ levels.
Conclusions:
- Non-mitochondrial synaptosomal Ca2+-ATPase likely plays a significant role in regulating intracellular calcium levels.
- Enzyme active sites appear to be located on the cytosolic face of membranes.
- External potassium suggests involvement of Ca2+ influx in ATPase activity regulation.
More Related Videos
17:05Loading a Calcium Dye into Frog Nerve Endings Through the Nerve Stump: Calcium Transient Registration in the Frog Neuromuscular Junction
Published on: July 8, 2017
09:07Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
Published on: February 18, 2020
Related Concept Videos
The Role of Ion Channels in Neuronal Computation
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.
Chemical Synapses
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...
Feedback Regulation of Calcium Concentration
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Calmodulin-dependent Signaling
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 Mechanism
Relaxation of Skeletal Muscles
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.