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Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine.

A Kirkwood1, C Rozas, J Kirkwood

  • 1Mind Brain Institute, Johns Hopkins University, Baltimore, Maryland 21218, USA.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|February 19, 1999
PubMed
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Cholinergic and noradrenergic modulators facilitate homosynaptic long-term depression (LTD) in rat visual cortex. This process, induced by paired-pulse stimulation (PPS), enhances receptive field plasticity.

Area of Science:

  • Neuroscience
  • Synaptic Plasticity
  • Cortical Circuits

Background:

  • Homosynaptic long-term depression (LTD) is a key mechanism for synaptic plasticity.
  • Cholinergic and noradrenergic systems modulate cortical function and plasticity.

Purpose of the Study:

  • To investigate the role of carbachol (CCh) and norepinephrine (NE) in inducing LTD in rat visual cortex.
  • To elucidate the receptor mechanisms and NMDA dependence of CCh- and NE-facilitated LTD.

Main Methods:

  • Slice preparation of rat visual cortex.
  • Paired-pulse stimulation (PPS) with concurrent application of CCh or NE.
  • Pharmacological blockade of specific receptors (M1, alpha1) and NMDA receptors.

Main Results:

Related Experiment Videos

  • PPS with CCh or NE induced homosynaptic LTD in superficial layers.
  • This LTD was comparable to low-frequency stimulation (LFS) but required fewer pulses.
  • Cholinergic facilitation involved M1 receptors; noradrenergic facilitation involved alpha1 receptors.
  • NMDA receptor blockers inhibited LTD induction, indicating modulation of NMDA receptor gain.

Conclusions:

  • Cholinergic and noradrenergic inputs facilitate NMDA receptor-dependent homosynaptic LTD.
  • This mechanism contributes to the modulation of receptive field plasticity in the neocortex.