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Study of the Functions and Activities of Neuronal K-Cl Co-Transporter KCC2 Using Western Blotting
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APP modulates KCC2 expression and function in hippocampal GABAergic inhibition.

Ming Chen1, Jinzhao Wang1, Jinxiang Jiang2,3

  • 1School of Life Sciences, South China Normal University, Guangzhou, China.

Elife
|January 6, 2017
PubMed
Summary

Amyloid precursor protein (APP) regulates GABAergic inhibition by interacting with KCC2, a transporter crucial for chloride homeostasis. APP deficiency impairs KCC2 function, affecting synaptic transmission in the hippocampus.

Keywords:
APPGABA reversal potentialIPSCKCC2hippocampusmouseneuroscienceprotein-protein interaction

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Synaptic Plasticity

Background:

  • Amyloid precursor protein (APP) is abundant at synapses, but its precise role in synaptic function remains unclear.
  • Previous studies indicated impaired GABAergic short-term plasticity in APP-deficient animals, suggesting a role in inhibitory neurotransmission.

Purpose of the Study:

  • To elucidate the molecular mechanism by which APP regulates GABAergic synaptic transmission.
  • To investigate the interaction between APP and the K+-Cl- cotransporter KCC2.

Main Methods:

  • Electrophysiological recordings of synaptic currents.
  • Biochemical assays to assess protein levels and interactions.
  • Moleculobiological and pharmacological analyses.

Main Results:

  • APP physically interacts with KCC2, essential for chloride homeostasis and GABAergic inhibition.
  • APP deficiency reduces KCC2 levels, depolarizing the GABA reversal potential (EGABA) and impairing inhibitory postsynaptic currents (IPSCs).
  • APP limits KCC2 tyrosine-phosphorylation and ubiquitination, thereby preventing its degradation.

Conclusions:

  • APP regulates GABAergic inhibition in the hippocampus through physical interaction with KCC2.
  • This interaction influences KCC2 abundance and function, impacting GABAAR mediated inhibition.
  • APP's role in maintaining KCC2 stability is critical for proper synaptic function.