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Calmodulin-dependent Signaling01:16

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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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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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Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Calmodulin as a major calcium buffer shaping vesicular release and short-term synaptic plasticity: facilitation

Yulia Timofeeva1, Kirill E Volynski2

  • 1Department of Computer Science, University of Warwick Coventry, UK ; Centre for Complexity Science, University of Warwick Coventry, UK.

Frontiers in Cellular Neuroscience
|July 21, 2015
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Summary

Calmodulin, a key calcium buffer in neurons, significantly inhibits synaptic vesicle release and shapes short-term plasticity. A new model suggests calmodulin

Keywords:
calcium channelsmodeling biological systemsshort-term plasticitysynaptic transmissionsynaptic vesicles

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Area of Science:

  • Neuroscience
  • Computational Biology
  • Cellular Signaling

Background:

  • Synaptic vesicle release and short-term plasticity are regulated by presynaptic calcium (Ca2+) dynamics.
  • Endogenous Ca2+ buffers, like calmodulin, shape these Ca2+ profiles but their direct impact on release is not fully understood.
  • Calmodulin is abundant and binds Ca2+ rapidly, suggesting a significant role in presynaptic function.

Purpose of the Study:

  • To investigate the direct effects of calmodulin on fast presynaptic Ca2+ dynamics.
  • To determine calmodulin's role in regulating synaptic vesicle release and short-term synaptic plasticity.
  • To explore novel mechanisms of synaptic plasticity involving calmodulin.

Main Methods:

  • Developed and utilized experimentally constrained three-dimensional diffusion modeling.
  • Simulated Ca2+ influx-exocytosis coupling at small excitatory synapses.
  • Analyzed the impact of calmodulin buffering at physiologically relevant concentrations.

Main Results:

  • Calmodulin buffering plays a dominant role in inhibiting vesicular release at synapses.
  • Calmodulin significantly modulates short-term synaptic plasticity.
  • Proposed a novel mechanism for short-term facilitation involving Ca2+-dependent calmodulin dislocation from the plasma membrane.

Conclusions:

  • Calmodulin is a critical determinant of synaptic transmission efficacy and plasticity.
  • The rapid Ca2+ buffering by calmodulin shapes presynaptic Ca2+ signals, controlling vesicle release.
  • Dynamic calmodulin-membrane interactions offer a new perspective on synaptic facilitation.