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Related Concept Videos

Excitatory and Inhibitory Effects of Neurotransmitters01:29

Excitatory and Inhibitory Effects of Neurotransmitters

When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
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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...
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Synaptic integration mainly includes the summation of graded potentials. Graded potentials, regardless of their type, cause subtle alterations in membrane voltage, resulting in either depolarization or hyperpolarization. These incremental changes, when combined or summed, can propel the neuron toward its threshold. Consider, for example, a membrane experiencing a +15 mV shift, causing it to depolarize from -70 mV to -55 mV. In this scenario, graded potentials govern the membrane's ability to...
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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
Hebbian LTP
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Updated: Jun 3, 2026

Inducing Plasticity of Astrocytic Receptors by Manipulation of Neuronal Firing Rates
12:47

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Published on: March 20, 2014

Glutamate released spontaneously from astrocytes sets the threshold for synaptic plasticity.

Christian Bonansco1, Alejandro Couve, Gertrudis Perea

  • 1Departamento de Fisiología, Universidad de Valparaíso, Valparaíso, Chile. christian.bonansco@uv.cl

The European Journal of Neuroscience
|March 15, 2011
PubMed
Summary

Spontaneous astrocyte activity, through glutamate release, regulates neurotransmitter release probability at central synapses. This astrocyte-derived glutamate acts via metabotropic glutamate receptors, influencing synaptic plasticity and information transfer.

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Last Updated: Jun 3, 2026

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Published on: March 20, 2014

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Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices
16:38

Dual Electrophysiological Recordings of Synaptically-evoked Astroglial and Neuronal Responses in Acute Hippocampal Slices

Published on: November 26, 2012

Area of Science:

  • Neuroscience
  • Cellular Neuroscience
  • Synaptic Plasticity

Background:

  • Astrocytes exhibit spontaneous calcium oscillations.
  • These oscillations may lead to glutamate release (gliotransmission).
  • The role of astrocytic glutamate in basal neurotransmitter release probability is unclear.

Purpose of the Study:

  • Investigate the impact of spontaneous astrocyte activity on neurotransmission.
  • Determine the effect of astrocytic glutamate release on synaptic plasticity.
  • Elucidate the mechanisms by which astrocytes modulate synaptic function.

Main Methods:

  • Whole-cell recordings in rat hippocampal slices.
  • Calcium imaging to monitor astrocytic activity.
  • Application of metabolic gliotoxin fluorocitrate (FC) and glutamine.
  • Pharmacological manipulation of metabotropic glutamate receptors and calcium signaling.

Main Results:

  • Fluorocitrate (FC) reduced excitatory postsynaptic current amplitude and increased paired-pulse facilitation, indicating decreased neurotransmitter release probability.
  • FC decreased astrocytic intracellular calcium signaling and glutamate release.
  • Blockade of group I metabotropic glutamate receptors mimicked FC's effects on miniature synaptic responses.
  • FC impaired spike-timing-dependent plasticity, which was rescued by stronger stimulation.

Conclusions:

  • Spontaneous astrocyte glutamate release modulates basal neurotransmitter release probability.
  • Metabotropic glutamate receptor activation by astrocytic glutamate acts as a gain control mechanism.
  • Astrocyte activity is critical for regulating synaptic plasticity and information transfer in the central nervous system.