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Published on: November 11, 2017
Synaptic lability after experience-dependent plasticity is not mediated by calcium-permeable AMPARs
1Department of Biological Sciences and Center for the Neural Basis of Cognition, Carnegie Mellon University, Pittsburgh PA, USA.
Frontiers in Molecular Neuroscience
|March 7, 2012
Summary
Calcium-permeable AMPARs do not cause synaptic instability after whisker experience. Synaptic depression can occur without these receptors, suggesting they are not essential for plasticity in the somatosensory cortex.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Receptor Trafficking
Background:
- Activity-dependent plasticity involves trafficking of calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs).
- CP-AMPARs can be transiently present and removed in an activity-dependent manner.
- Previous work showed single-whisker experience (SWE) strengthens cortical synapses via CP-AMPARs, but this potentiation is labile.
Purpose of the Study:
- To test if CP-AMPARs confer instability onto recently potentiated synapses.
- To evaluate the role of CP-AMPARs in synaptic instability after in vivo plasticity.
- To dissociate the presence of CP-AMPARs from synaptic depression mechanisms.
Main Methods:
- Developed a strontium-depression assay to weaken individual synapses after SWE.
- Used strontium-replaced artificial cerebrospinal fluid (ACSF) to induce depression.
- Measured changes in excitatory postsynaptic current (EPSC) amplitude and event frequency.
Main Results:
- Sr-depression rapidly reduced EPSC amplitude without altering event frequency, indicating postsynaptic changes.
- N-methyl-D-aspartate receptor (NMDAR) activation was required for Sr-depression.
- Sr-depression occurred even when CP-AMPARs were absent, and CP-AMPARs were present in some control synapses without depression.
Conclusions:
- CP-AMPARs are neither sufficient nor necessary for synaptic depression following in vivo plasticity in the somatosensory cortex.
- Synaptic instability after plasticity may involve mechanisms independent of CP-AMPAR presence.
- Findings challenge the direct link between CP-AMPARs and labile synapses in this context.
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