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Related Concept Videos

Excitatory and Inhibitory Effects of Neurotransmitters01:29

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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...
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory 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.
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Long-term Potentiation01:25

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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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Diffusion dynamics of synaptic molecules during inhibitory postsynaptic plasticity.

Enrica Maria Petrini1, Andrea Barberis1

  • 1Department of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia Genoa, Italy.

Frontiers in Cellular Neuroscience
|October 9, 2014
PubMed
Summary

Investigating inhibitory synaptic plasticity reveals that postsynaptic mechanisms, involving GABAergic synapse molecular reorganization, are crucial for modulating neuronal networks. Protein dynamics drive these activity-dependent adjustments in synaptic strength.

Keywords:
GABAA receptorsGABAergic plasticitygephyrinintracellular traffickinglateral diffusionphosphorylationscaffold proteinssingle particle tracking

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Inhibitory transmission plasticity modulates neuronal excitability and network function.
  • Presynaptic mechanisms of inhibitory synaptic plasticity are well-characterized.
  • Postsynaptic mechanisms remain less understood, despite their importance.

Purpose of the Study:

  • To review the molecular mechanisms underlying postsynaptic inhibitory synaptic plasticity.
  • To highlight the dynamic reorganization of the GABAergic synapse.
  • To emphasize the role of protein dynamics in synaptic strength modulation.

Main Methods:

  • Review of existing literature on inhibitory synaptic plasticity.
  • Analysis of molecular components of the GABAergic synapse.
  • Focus on postsynaptic mechanisms involving receptor trafficking and scaffold proteins.

Main Results:

  • Postsynaptic plasticity involves rearrangement of GABAA receptors, scaffold proteins, and structural molecules.
  • Dynamic modulation of receptor trafficking and lateral diffusion is essential.
  • Regulation of scaffold protein availability and distribution is a key factor.

Conclusions:

  • Postsynaptic mechanisms are critical for inhibitory long-term synaptic plasticity.
  • Protein dynamics orchestrate the molecular reorganization of inhibitory synapses.
  • These processes ensure reliable, activity-dependent adjustments of synaptic strength.