Abstract / Description of output
A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.
| Original language | English |
|---|---|
| Pages (from-to) | 12852-12857 |
| Number of pages | 6 |
| Journal | Proceedings of the National Academy of Sciences (PNAS) |
| Volume | 112 |
| Issue number | 41 |
| Early online date | 28 Sept 2015 |
| DOIs | |
| Publication status | Published - 13 Oct 2015 |
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Emily Osterweil
- Centre for Discovery Brain Sciences
- Edinburgh Neuroscience
- Deanery of Biomedical Sciences - UoE Honorary staff
Person: Academic: Research Active , Affiliated Independent Researcher