Related Experiment Video
Updated: Aug 12, 2026

08:38
Vibrodissociation of Neurons from Rodent Brain Slices to Study Synaptic Transmission and Image Presynaptic Terminals
Published on: May 25, 2011
Calcium-stimulated adenosine triphosphatases in synaptic membranes
Journal of Neurochemistry
|December 1, 1981
Summary
Researchers studied ATPases in rat brain synapses, identifying a calcium-dependent ATPase potentially involved in calcium transport. This enzyme, enhanced by calmodulin, shows specific inhibition by agents like vanadate.
Area of Science:
- Neuroscience
- Biochemistry
- Cell Biology
Background:
- Synaptic membranes contain various ATPases crucial for neuronal function.
- Understanding these enzymes is key to elucidating neurotransmission and calcium homeostasis.
Purpose of the Study:
- To characterize ATPases in rat cerebral cortex synaptic membranes.
- To identify potential calcium-transporting ATPases within these preparations.
Main Methods:
- Enzyme activity assays on synaptic membrane preparations.
- Investigated Mg2+-ATPase, Ca2+-dependent ATPases, and calmodulin-stimulated activity.
- Utilized specific inhibitors like vanadate and La3+ for characterization.
Main Results:
- Identified intrinsic (Na+ + K+)-ATPase and contaminating Mg2+-ATPase.
- Characterized a Mg2+-ATPase, a high-concentration Ca2+-dependent ATPase, and a high-affinity (Ca2+ + Mg2+)-ATPase.
- The (Ca2+ + Mg2+)-ATPase activity was significantly enhanced by calmodulin.
- Specific inhibitors like vanadate and La3+ selectively inhibited the (Ca2+ + Mg2+)-ATPase.
Conclusions:
- The characterized (Ca2+ + Mg2+)-ATPase, particularly its calmodulin-stimulated form, exhibits properties consistent with a role in neuronal calcium transport.
- This enzyme may be critical for regulating intracellular calcium levels in nerve endings.
More Related Videos
Related Concept Videos
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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...
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...
IP3/DAG Signaling Pathway
Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and produces two-second...
Feedback Regulation of Calcium Concentration
Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
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
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,...
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
Relaxation of Skeletal Muscles
The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
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.
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.
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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...
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...

