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Related Experiment Videos

Persistent signalling and changes in presynaptic function in long-term potentiation.

A Malgaroli1, R Malinow, H Schulman

  • 1Department of Molecular and Cellular Physiology, Stanford University Medical Center, CA 94305-5425.

Ciba Foundation Symposium
|January 1, 1992
PubMed
Summary
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Long-term potentiation (LTP) in the brain requires protein kinase C (PKC) and Ca2+/calmodulin-dependent protein kinase II (CaMKII) for its induction. However, established LTP expression appears to involve a presynaptic mechanism, suggesting a retrograde signal.

Area of Science:

  • Neuroscience
  • Cellular and Molecular Biology

Background:

  • Long-term potentiation (LTP) is a persistent change in synaptic function crucial for learning and memory in mammals.
  • LTP at hippocampal CA3-CA1 synapses is induced by calcium (Ca2+) influx via NMDA receptors.

Purpose of the Study:

  • To investigate the role of Ca2+-dependent protein kinases in the induction and expression of LTP.
  • To determine the cellular locus (postsynaptic vs. presynaptic) of LTP expression.

Main Methods:

  • Intracellular injection of specific inhibitory peptide blockers for protein kinase C (PKC) and Ca2+/calmodulin-dependent protein kinase II (CaMKII).
  • Whole-cell voltage clamp recordings to study quantal synaptic transmission.
  • Analysis of miniature synaptic currents in hippocampal cultures.

Related Experiment Videos

Main Results:

  • Inhibition of both PKC and CaMKII prevented LTP induction, indicating their necessity for postsynaptic induction.
  • Established LTP was not suppressed by intracellular kinase inhibitors, but remained sensitive to bath application, suggesting a presynaptic locus.
  • Studies of synaptic transmission showed enhanced presynaptic release but no increase in quantal size, supporting presynaptic expression.

Conclusions:

  • Both PKC and CaMKII are essential for the postsynaptic induction of LTP.
  • LTP expression likely occurs at the presynaptic terminal, requiring a retrograde signal from the postsynaptic neuron.
  • The persistent signal for LTP expression may involve a kinase not accessible within the postsynaptic cell.