Related Experiment Video
Updated: Jun 6, 2026
12:47
Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
Published on: March 20, 2014
Is astrocyte calcium signaling relevant for synaptic plasticity?
Sarrah Ben Achour1, Lorena Pont-Lezica, Catherine Béchade
1Ecole Normale Supérieure, Institut de Biologie de l'ENS, IBENS, Paris, France.
Neuron Glia Biology
|December 3, 2010
Summary
Calcium signaling in astrocytes is crucial for neuronal communication and synaptic plasticity. This review explores calcium
Area of Science:
- Neuroscience
- Cell Biology
- Glial Cell Research
Background:
- Astrocytes, once viewed as passive support cells for neurons, are now recognized for their active role in brain function.
- Calcium signaling within astrocytes has emerged as a key mechanism for intercellular communication and regulating astrocyte physiology.
- Initial studies demonstrated direct astrocyte-neuron interactions via calcium waves, highlighting astrocytes' involvement in information processing.
Purpose of the Study:
- To review the diverse mechanisms governing calcium flux in astrocytes.
- To outline calcium-dependent pathways for gliotransmitter release.
- To critically examine the role of calcium in synaptic plasticity and reconcile conflicting findings.
Main Methods:
- Literature review of studies on astrocyte calcium signaling.
- Analysis of mechanisms controlling calcium influx and efflux in astrocytes.
- Synthesis of data on calcium-mediated gliotransmitter release and synaptic plasticity.
Main Results:
- Astrocytes exhibit complex calcium dynamics influencing neuronal activity.
- Calcium-dependent gliotransmitter release plays a role in modulating synaptic transmission.
- Evidence for calcium's role in synaptic plasticity is inconsistent, suggesting involvement of other factors.
Conclusions:
- Astrocytes are integral to synaptic function and plasticity through sophisticated calcium signaling.
- Further research is needed to fully elucidate the precise role of astrocyte calcium in synaptic plasticity.
- Alternative explanations are proposed to reconcile discrepancies in current research findings.
More Related Videos
16:38Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices
Published on: November 26, 2012
12:19Imaging Intracellular Ca2+ Signals in Striatal Astrocytes from Adult Mice Using Genetically-encoded Calcium Indicators
Published on: November 19, 2014
Related Concept Videos
01:26Chemical 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...
01:26Chemical 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...
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...
01:09Synaptic Signaling
Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
Most synapses are chemical, meaning an electrical impulse or action potential spurs the release of chemical messengers called neurotransmitters. The neuron sending the signal is called the presynaptic neuron, and the neuron receiving the signal is the postsynaptic neuron.
The presynaptic neuron fires an action potential that...
01:12Synaptic Signaling
Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
01:16Calmodulin-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,...