ArticleJournal of computational neuroscience2010
Possible role of cooperative action of NMDA receptor and GABA function in developmental plasticity.
Article in Journal of computational neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 13 citations in OpenAlex.
- A Practical Guide to SparseFrontiers in neuroscience · 2021Article
- A Primer on Constructing Plasticity Phenotypes to Classify Experience-Dependent Development of the Visual Cortex.Frontiers in cellular neuroscience · 2020Article
- Postsynaptic signal transduction models for long-term potentiation and depression.Frontiers in computational neuroscience · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
The maturation of cortical circuits is strongly influenced by sensory experience during a restricted critical period. The developmental alteration in the subunit composition of NMDA receptors (NMDARs) has been suggested to be involved in regulating the timing of such plasticity. However, this hypothesis does not explain the evidence that enhancing GABA inhibition triggers a critical period in the visual cortex. Here, to investigate how the NMDAR and GABA functions influence synaptic organization, we examine an spike-timing-dependent plasticity (STDP) model that incorporates the dynamic modulation of LTP, associated with the activity- and subunit-dependent desensitization of NMDARs, as well as the background inhibition by GABA. We show that the competitive interaction between correlated input groups, required for experience-dependent synaptic modifications, may emerge when both the NMDAR subunit expression and GABA inhibition reach a sufficiently mature state. This may suggest that the cooperative action of these two developmental mechanisms can contribute to embedding the spatiotemporal structure of input spikes in synaptic patterns and providing the trigger for experience-dependent cortical plasticity.
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