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Long-lasting potentiation and depression without presynaptic activity

D Neveu1, R S Zucker

  • 1Neurobiology Division, University of California, Berkeley 94720, USA.

Journal of Neurophysiology
|May 1, 1996
PubMed
Summary
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A rise in postsynaptic intracellular calcium (Ca2+) is sufficient for inducing long-term potentiation and depression. This finding demonstrates that presynaptic activity is not required for these crucial synaptic plasticity mechanisms.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Synaptic Plasticity

Background:

  • Long-term potentiation (LTP) and long-term depression (LTD) are key forms of synaptic plasticity.
  • Both LTP and LTD are known to require a rise in postsynaptic intracellular calcium concentration ([Ca2+]i).
  • The necessity of concurrent presynaptic activity for LTP/LTD induction and expression remains unclear.

Purpose of the Study:

  • To investigate whether postsynaptic calcium increase alone is sufficient for LTP and LTD.
  • To determine if presynaptic activity is essential for the induction and expression of these synaptic changes.

Main Methods:

  • Utilized photolysis of a caged-calcium compound (nit-5) to precisely elevate postsynaptic [Ca2+]i.
  • Induced long-lasting potentiation (LLP) and long-lasting depression (LLD) in CA1 pyramidal neurons.

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Main Results:

  • Successfully induced LLP and LLD solely by increasing postsynaptic [Ca2+]i.
  • Achieved these synaptic modifications in the complete absence of presynaptic activity.
  • Observed that the induced LLP and LLD shared characteristics with conventionally induced LTP and LTD.

Conclusions:

  • A rise in postsynaptic [Ca2+]i is both necessary and sufficient for LTP and LTD induction and expression.
  • Concurrent presynaptic activity is not required for these forms of synaptic plasticity.
  • These findings refine our understanding of the molecular mechanisms underlying synaptic plasticity.