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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.
Summary
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:
- 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.
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