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Long term depression in the CA1 field is associated with a transient decrease in pre- and postsynaptic PKC substrate

G M Ramakers1, K Heinen, W H Gispen

  • 1Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Universiteitsweg 100, 3584 CG Utrecht, The Netherlands. g.j.j.ramakers@med.uu.nl

The Journal of Biological Chemistry
|June 27, 2000
PubMed
Summary
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Long-term depression (LTD) in the hippocampus involves increased phosphatase activity, reducing phosphorylation of key proteins like GAP-43/B-50 and RC3. This suggests phosphatases link calcium signals to synaptic plasticity.

Area of Science:

  • Neuroscience
  • Cellular and Molecular Biology
  • Synaptic Plasticity

Background:

  • Long-term depression (LTD) in the hippocampus (CA1 field) is a crucial form of synaptic plasticity.
  • LTD is believed to depend on N-methyl-d-aspartate receptor activation, increased postsynaptic calcium, and enhanced phosphatase activity.

Purpose of the Study:

  • To investigate the spatial and temporal dynamics of protein phosphatase activity during LTD induction.
  • To determine the role of specific protein substrates in linking calcium signaling to LTD.

Main Methods:

  • Used rat hippocampal slices to study N-methyl-d-aspartate receptor-dependent LTD.
  • Assessed the in situ phosphorylation state of pre- and postsynaptic protein kinase C substrates (GAP-43/B-50 and RC3).
  • Utilized phosphatase inhibitors (okadaic acid, cyclosporin A) and an N-methyl-d-aspartate receptor antagonist (D-AP5).

Related Experiment Videos

Main Results:

  • LTD induction was associated with a transient (<30 min) and D-AP5-sensitive reduction in GAP-43/B-50 and RC3 phosphorylation.
  • Inhibition of phosphatases with okadaic acid or cyclosporin A prevented LTD.
  • Demonstrated a transient increase in both pre- and postsynaptic phosphatase activity during LTD.

Conclusions:

  • Provided strong evidence for a transient increase in phosphatase activity during hippocampal LTD.
  • Phosphorylation changes in calmodulin-binding proteins GAP-43/B-50 and RC3 occur during LTD.
  • These proteins may mediate the link between calcium influx and downstream signaling pathways involved in synaptic plasticity (LTD and LTP).