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It is essential to understand how structural members behave under plastic deformation when the bending stress exceeds the material's yield strength. This state of deformation permanently alters the shape of the member, in contrast to the linear elastic behavior observed before yielding. The strain at any point in the member is expressed in terms of maximum strain. Notably, the neutral axis, which coincides with the centroid during elastic bending, shifts away from the centroid under plastic...
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Related Experiment Video

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Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae
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Neuronal TDP-43 depletion affects activity-dependent plasticity.

Paulina Koza1, Anna Beroun1, Anna Konopka2

  • 1Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.

Neurobiology of Disease
|June 10, 2019
PubMed
Summary

TAR DNA-binding protein 43 (TDP-43) depletion in neurons enhances fear memory acquisition and alters synaptic plasticity. TDP-43 regulates RNA splicing, impacting neuronal excitability and synaptic function in neurodegenerative diseases.

Keywords:
AMPA receptorsFLOP/FLIP splice variantsPTZ modelTDP-43

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • TAR DNA-binding protein 43 (TDP-43) is implicated in neurodegenerative diseases like ALS and FTD.
  • TDP-43 pathology involves abnormal protein aggregates and dysfunction in RNA processing.
  • The precise physiological role of TDP-43 in neuronal function and degeneration is not fully understood.

Purpose of the Study:

  • To investigate the role of TDP-43 in neuronal plasticity and memory.
  • To explore the molecular mechanisms underlying TDP-43's effects on synaptic function.

Main Methods:

  • Utilized transgenic rats with neuron-specific TDP-43 depletion.
  • Assessed fear memory acquisition and fear conditioning.
  • Performed electrophysiological recordings to evaluate intrinsic neuronal excitability and synaptic plasticity (long-term potentiation) in the hippocampus.
  • Analyzed protein levels of AMPA receptor subunits (GluR1, GluR2/3) and assessed AMPAR kinetics.

Main Results:

  • TDP-43 depletion enhanced fear memory acquisition.
  • TDP-43-depleted neurons showed reduced short-term plasticity of intrinsic neuronal excitability.
  • Long-term potentiation in the hippocampus (CA3-CA1) was more stable with TDP-43 depletion.
  • Decreased protein levels of unedited (R) FLOP variants of GluR1 and GluR2/3 AMPA receptor subunits were observed.
  • Altered FLOP/FLIP subunit composition affected AMPAR kinetics, indicated by slowed miniature excitatory postsynaptic current decay.

Conclusions:

  • TDP-43 plays a role in regulating activity-dependent neuronal plasticity.
  • TDP-43 may influence fast synaptic transmission and membrane potential by regulating gene splicing.
  • Findings suggest TDP-43's involvement in the molecular pathways underlying neurodegenerative conditions affecting memory and neuronal function.