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Related Experiment Videos

Post-receptor mechanisms underlying striatal long-term depression

P Calabresi1, A Pisani, N B Mercuri

  • 1Clinica Neurologica, Dip. Sanità, Università di Tor Vergata, Rome, Italy.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|August 1, 1994
PubMed
Summary

Post-tetanic long-term depression (LTD) in the striatum requires calcium influx via nifedipine-sensitive channels and activation of calcium-dependent protein kinases for motor memory formation.

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Area of Science:

  • Neuroscience
  • Cellular Neuroscience
  • Synaptic Plasticity

Background:

  • Striatal post-tetanic long-term depression (LTD) is a form of synaptic plasticity crucial for motor learning.
  • Understanding the post-receptor mechanisms of striatal LTD is essential for elucidating its role in motor memory.

Purpose of the Study:

  • To characterize the post-receptor mechanisms underlying striatal LTD.
  • To investigate the role of calcium (Ca2+) influx and Ca2+-dependent protein kinases in striatal LTD.

Main Methods:

  • Extracellular and intracellular recordings from striatal neurons in brain slices.
  • Utilized calcium chelators (BAPTA, EGTA) and QX-314 to block ion channels.
  • Applied nifedipine to block L-type Ca2+ channels and kinase inhibitors (staurosporine, H-7, calphostin C).

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Main Results:

  • Striatal LTD was blocked by calcium chelators and QX-314, but restored by depolarization.
  • Nifedipine, an L-type Ca2+ channel blocker, abolished striatal LTD.
  • Inhibitors of Ca2+-dependent protein kinases reduced or blocked striatal LTD.

Conclusions:

  • Striatal LTD generation necessitates Ca2+ influx through voltage-dependent, nifedipine-sensitive channels.
  • Sufficient intracellular free Ca2+ concentration and activation of Ca2+-dependent protein kinases are critical for striatal LTD.
  • Modulation of striatal LTD by drugs may impact motor memory formation.