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Long-term potentiation in mice lacking synapsins

D M Spillane1, T W Rosahl, T C Südhof

  • 1Department of Psychiatry, University of California, San Francisco 94143-0984, USA.

Neuropharmacology
|November 1, 1995
PubMed
Summary

Synapsins are not essential for synaptic plasticity or transmission. Studies in knockout mice show normal long-term potentiation and responses to protein kinase modulators, excluding these phosphoproteins from key roles.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Cell Biology

Background:

  • Synapsins I and II are abundant synaptic vesicle phosphoproteins.
  • They are proposed to be crucial for synaptic transmission and plasticity.
  • Their phosphorylation sites' functional significance remains unclear.

Purpose of the Study:

  • To investigate the role of synapsins in synaptic transmission and plasticity.
  • To determine the necessity of synapsins for protein kinase-mediated synaptic processes.

Main Methods:

  • Utilized knockout mice lacking both synapsin I and synapsin II.
  • Examined long-term potentiation (LTP) in hippocampal slices (mossy fiber-CA3 and Schaffer collateral-CA1 synapses).
  • Assessed synaptic transmission changes induced by forskolin and H-7.

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Main Results:

  • Long-term potentiation (LTP) was normal in hippocampal slices from synapsin-deficient mice.
  • Synaptic transmission changes induced by forskolin (PKA activator) and H-7 were unaffected in mutant mice.
  • Synapsins are not required for LTP induction or expression.

Conclusions:

  • Synapsins are not essential for hippocampal long-term potentiation.
  • These phosphoproteins do not play a necessary role in cAMP-dependent protein kinase (PKA) mediated enhancement of transmitter release.
  • Synapsins are not required for H-7-induced depression of synaptic transmission.
  • The most abundant synaptic phosphoproteins are excluded as essential for long-term synaptic plasticity.