ArticleDevelopmental neurobiology2010
Synaptic drive at developing synapses: transient upregulation of kainate receptors.
Article in Developmental neurobiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 0 citations in OpenAlex.
- Biflorin Ameliorates Memory Impairments Induced by Cholinergic Blockade in Mice.Biomolecules & therapeutics · 2017Article
- Deactivation kinetics of acid-sensing ion channel 1a are strongly pH-sensitive.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Illuminating the multifaceted roles of neurotransmission in shaping neuronal circuitry.Neuron · 2014Review
- A Myosin Va mutant mouse with disruptions in glutamate synaptic development and mature plasticity in visual cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
At the onset of a period of intense synaptic refinement initiated by synchronized eye opening (EO), rapid changes in postsynaptic NMDA receptor and AMPA receptor currents (NMDARcs and AMPARcs) occur within the superficial visual layers of the rodent superior colliculus (sSC; Lu and Constantine-Paton [2004]: Neuron 43:237-249). Subsequently, evoked non-NMDARc amplitudes increase, but by 2 weeks after EO (AEO) they decrease significantly. Here, using whole-cell patch-clamp recording, we demonstrate that small, slowly desensitizing excitatory kainate receptor currents (KARcs) are responsible for the rise and subsequent fall in non-NMDARcs. The increase in KAR transmission parallels inhibitory GABA(A) responses that plateau at 7 days AEO. By 2 weeks AEO, KARcs are gone. AMPARcs remain unchanged during the appearance and disappearance of the KARcs, despite increases in sSC neuropil activity and continued refinement of inputs to individual sSC neurons. We suggest that in the interval of heightened activity, before SC inhibition matures, many AMPARcs desensitize and are relatively ineffective at relieving the Mg(2+) block on NMDARs. This transient appearance of slowly desensitizing, long-duration KARcs may provide increased membrane depolarization necessary for NMDAR function and continuation of synaptic refinement.
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