ArticleNature communications2017
Input-dependent regulation of excitability controls dendritic maturation in somatosensory thalamocortical neurons.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Gene-environmental regulation of the postnatal post-mitotic neuronal maturation.Trends in genetics : TIG · 2024Review
- Potential Roles for the GluN2D NMDA Receptor Subunit in Schizophrenia.International journal of molecular sciences · 2023Review
- Targeting NMDA Receptors at the Neurovascular Unit: Past and Future Treatments for Central Nervous System Diseases.International journal of molecular sciences · 2022Review
- Bottom-up inputs are required for establishment of top-down connectivity onto cortical layer 1 neurogliaform cells.Neuron · 2021Article
- 5-HT6R null mutatrion induces synaptic and cognitive defects.Aging cell · 2021Article
- Loss of Ryanodine Receptor 2 impairs neuronal activity-dependent remodeling of dendritic spines and triggers compensatory neuronal hyperexcitability.Cell death and differentiation · 2020Article
- Article
- NMDA receptor hypofunction for schizophrenia revisited: Perspectives from epigenetic mechanisms.Schizophrenia research · 2020Review
- TREK-1 Null Impairs Neuronal Excitability, Synaptic Plasticity, and Cognitive Function.Molecular neurobiology · 2020Article
- The origin of NMDA receptor hypofunction in schizophrenia.Pharmacology & therapeutics · 2020Review
- GluN2B but Not GluN2A for Basal Dendritic Growth of Cortical Pyramidal Neurons.Frontiers in neuroanatomy · 2020Article
- Dynamic Regulation of Synaptopodin and the Axon Initial Segment in Retinal Ganglion Cells During Postnatal Development.Frontiers in cellular neuroscience · 2019Article
- SK Channel Modulates Synaptic Plasticity by Tuning CaMKIIα/β Dynamics.Frontiers in synaptic neuroscience · 2019Article
- Development of tactile sensory circuits in the CNS.Current opinion in neurobiology · 2018Review
- Dendrite morphogenesis from birth to adulthood.Current opinion in neurobiology · 2018Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Input from the sensory organs is required to pattern neurons into topographical maps during development. Dendritic complexity critically determines this patterning process; yet, how signals from the periphery act to control dendritic maturation is unclear. Here, using genetic and surgical manipulations of sensory input in mouse somatosensory thalamocortical neurons, we show that membrane excitability is a critical component of dendritic development. Using a combination of genetic approaches, we find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal development leads to epigenetic repression of Kv1.1-type potassium channels, increased excitability, and impaired dendritic maturation. Lesions to whisker input pathways had similar effects. Overexpression of Kv1.1 was sufficient to enable dendritic maturation in the absence of sensory input. Thus, Kv1.1 acts to tune neuronal excitability and maintain it within a physiological range, allowing dendritic maturation to proceed. Together, these results reveal an input-dependent control over neuronal excitability and dendritic complexity in the development and plasticity of sensory pathways.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.