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Homosynaptic long-term depression in the visual cortex

A Kirkwood1, M F Bear

  • 1Department of Neuroscience, Brown University, Providence, Rhode Island 02912.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|May 1, 1994
PubMed
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Low-frequency stimulation induces long-term depression (LTD) in visual cortex, a homosynaptic process dependent on NMDA receptors and protein phosphatases. This synaptic weakening mechanism is similar to that observed in the hippocampus.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Visual Cortex Research

Background:

  • Synaptic effectiveness can decrease with activity.
  • Understanding these mechanisms is crucial for brain function.

Purpose of the Study:

  • To investigate the characteristics and mechanism of activity-dependent decreases in synaptic effectiveness in the visual cortex.
  • To determine if low-frequency stimulation (LFS) induces long-term depression (LTD) in the visual cortex.

Main Methods:

  • Used visual cortical slices for electrophysiological recordings.
  • Applied repetitive low-frequency stimulation (LFS) to layer IV or white matter.
  • Monitored synaptic responses to independent pathways to assess homosynapticity.
  • Investigated the role of NMDA receptors and protein phosphatases (using okadaic acid).

Related Experiment Videos

Main Results:

  • LFS induced a homosynaptic long-term depression (LTD) of synaptic responses in layer III.
  • LTD was dependent on stimulation frequency/pattern and NMDA receptor activation.
  • Inhibition of protein phosphatases 1 and 2a prevented LTD induction.
  • LFS-induced LTD in visual cortex closely resembles hippocampal LTD.

Conclusions:

  • LTD in the visual cortex is triggered by postsynaptic Ca2+ elevation and protein-serine, threonine phosphatase activation.
  • The mechanism of LTD in visual cortex shares similarities with that in the hippocampus.
  • This study elucidates a key form of synaptic plasticity in the visual cortex.