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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.
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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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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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Fluorescent Calcium Imaging and Subsequent In Situ Hybridization for Neuronal Precursor Characterization in Xenopus laevis
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Simplified calcium signaling cascade for synaptic plasticity.

Vladimir Kornijcuk1, Dohun Kim2, Guhyun Kim2

  • 1Division of Materials Science and Engineering, Hanyang University, Wangsimni-ro 222, Seongdong-gu, 04763 Seoul, Republic of Korea.

Neural Networks : the Official Journal of the International Neural Network Society
|December 11, 2019
PubMed
Summary
This summary is machine-generated.

This study introduces a simplified chemical model for synaptic plasticity, focusing on calcium signaling and receptor modification. The model accurately simulates various plasticity protocols and ocular dominance, offering a tangible chemical basis for long-term changes.

Keywords:
Back-propagating action potential boostCalcium signaling cascadeSynaptic competitionSynaptic plasticity

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Area of Science:

  • Computational Neuroscience
  • Molecular Neuroscience
  • Systems Neuroscience

Background:

  • Synaptic plasticity underlies learning and memory.
  • Existing models often rely on abstract thresholds for calcium concentration.
  • A need exists for models grounded in tangible chemical reactions.

Purpose of the Study:

  • To propose a simplified model of synaptic plasticity based on a calcium signaling cascade.
  • To represent long-term plasticity using chemical reactions and fictive catalysts.
  • To move beyond conceptual theories like preset calcium concentration thresholds.

Main Methods:

  • Developed a model simplifying calcium influx to glutamate receptor phosphorylation (potentiation) and dephosphorylation (depression).
  • Incorporated fictive catalysts (C1 and C2) for potentiation and depression, respectively.
  • Simulated synaptic plasticity using chemical reaction principles.

Main Results:

  • The model successfully reproduced experimental synaptic plasticity under synchronous pairing protocols.
  • It also replicated plasticity induced by correlated presynaptic and postsynaptic action potentials (APs).
  • Ocular dominance plasticity was reproduced by competing synapses utilizing back-propagating APs (bAPs).

Conclusions:

  • The simplified chemical model provides a tangible basis for understanding long-term synaptic plasticity.
  • The model's ability to reproduce complex plasticity phenomena validates its approach.
  • Synapse-specific back-propagating APs are key to competitive plasticity dynamics.