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Related Concept Videos

Long-term Potentiation01:25

Long-term Potentiation

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
LTP can occur when presynaptic neurons...
Long-term Potentiation01:35

Long-term Potentiation

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.
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...
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for their...
Integration of Synaptic Events01:28

Integration of Synaptic Events

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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Whole-cell Currents Induced by Puff Application of GABA in Brain Slices
07:32

Whole-cell Currents Induced by Puff Application of GABA in Brain Slices

Published on: October 12, 2017

GABAergic circuits control spike-timing-dependent plasticity.

Vincent Paille1, Elodie Fino, Kai Du

  • 1Team Dynamic and Pathophysiology of Neuronal Networks, Center for Interdisciplinary Research in Biology, Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7241/INSERM U1050, College de France, 75005 Paris, France.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 31, 2013
PubMed
Summary
This summary is machine-generated.

GABAergic signaling, a key neurotransmitter pathway, dictates the direction of synaptic plasticity (STDP). Blocking GABAergic receptors reversed learning and memory encoding at corticostriatal synapses.

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Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration
07:08

Fast Micro-iontophoresis of Glutamate and GABA: A Useful Tool to Investigate Synaptic Integration

Published on: July 31, 2013

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Learning and Memory

Background:

  • Spike-timing-dependent plasticity (STDP) is crucial for learning and memory.
  • GABAergic signaling modulates neuronal excitability and spike timing.
  • The role of GABAergic circuits in governing STDP polarity was previously unknown.

Purpose of the Study:

  • To investigate whether GABAergic signaling circuits control the polarity of STDP.
  • To elucidate the mechanisms by which GABA influences STDP at corticostriatal synapses.

Main Methods:

  • Electrophysiological recordings in rats and mice.
  • Pharmacological blockade of GABAA receptors.
  • Biophysical simulations of neuronal activity.
  • Analysis of calcium dynamics involving NMDARs and voltage-sensitive calcium channels.

Main Results:

  • Blockade of GABAA receptors completely reversed the temporal order of STDP at corticostriatal synapses.
  • GABAergic signaling controls STDP polarity in both striatopallidal and striatonigral output neurons.
  • GABA's influence on STDP polarity is mediated by depolarizing effects at distal dendrites, altering calcium source balance.

Conclusions:

  • GABAergic circuits play a central role in shaping STDP.
  • GABAergic signaling acts as a switch, determining Hebbian or anti-Hebbian plasticity.
  • These findings reveal a novel mechanism for regulating synaptic plasticity and memory encoding.