ArticleBiological psychiatry2014
The dyslexia-associated gene DCDC2 is required for spike-timing precision in mouse neocortex.
Article in Biological psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 40 citations in OpenAlex.
- An assessment of gene-by-gene interactions as a tool to unfold missing heritability in dyslexia.Human genetics · 2015Trial
- Alterations in neural activation in the ventral frontoparietal network during complex magnocellular stimuli in developmental dyslexia associated with READ1 deletion.Behavioral and brain functions : BBF · 2024Article
- Genetic and protein interaction studies between the ciliary dyslexia candidate genes DYX1C1 and DCDC2.BMC molecular and cell biology · 2023Article
- Animal models of developmental dyslexia.Frontiers in neuroscience · 2022Review
- The Mediation Role of Dynamic Multisensory Processing Using Molecular Genetic Data in Dyslexia.Brain sciences · 2020Article
- Article
- Neuroimaging genetics studies of specific reading disability and developmental language disorder: A review.Language and linguistics compass · 2019Article
- The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on.The European journal of neuroscience · 2018Review
- Worldwide distribution of theProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Neurochemistry Predicts Convergence of Written and Spoken Language: A Proton Magnetic Resonance Spectroscopy Study of Cross-Modal Language Integration.Frontiers in psychology · 2018Article
- The role of READ1 and KIAA0319 genetic variations in developmental dyslexia: testing main and interactive effects.Journal of human genetics · 2017Article
- Enrichment of putatively damaging rare variants in the DYX2 locus and the reading-related genes CCDC136 and FLNC.Human genetics · 2017Article
- Rescue of impaired sociability and anxiety-like behavior in adult cacna1c-deficient mice by pharmacologically targeting eIF2α.Molecular psychiatry · 2017Article
- Neural Noise Hypothesis of Developmental Dyslexia.Trends in cognitive sciences · 2017Review
- Dyslexia risk gene relates to representation of sound in the auditory brainstem.Developmental cognitive neuroscience · 2017Article
- Normal radial migration and lamination are maintained in dyslexia-susceptibility candidate gene homolog Kiaa0319 knockout mice.Brain structure & function · 2017Article
- Neurogenetics of developmental dyslexia: from genes to behavior through brain neuroimaging and cognitive and sensorial mechanisms.Translational psychiatry · 2017Review
- Why is the processing of global motion impaired in adults with developmental dyslexia?Brain and cognition · 2016Article
- Mutation of the Dyslexia-Associated Gene Dcdc2 Enhances Glutamatergic Synaptic Transmission Between Layer 4 Neurons in Mouse Neocortex.Cerebral cortex (New York, N.Y. : 1991) · 2016Article
- Knockdown of Dyslexia-Gene Dcdc2 Interferes with Speech Sound Discrimination in Continuous Streams.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundVariants in dyslexia-associated genes, including DCDC2, have been linked to altered neocortical activation, suggesting that dyslexia associated genes might play as yet unspecified roles in neuronal physiology.
methodsWhole-cell patch clamp recordings were used to compare the electrophysiological properties of regular spiking pyramidal neurons of neocortex in Dcdc2 knockout (KO) and wild-type mice. Ribonucleic acid sequencing and reverse transcriptase polymerase chain reaction were performed to identify and characterize changes in gene expression in Dcdc2 KOs.
resultsNeurons in KOs showed increased excitability and decreased temporal precision in action potential firing. The RNA sequencing screen revealed that the N-methyl-D-aspartate receptor (NMDAR) subunit Grin2B was elevated in Dcdc2 KOs, and an electrophysiological assessment confirmed a functional increase in spontaneous NMDAR-mediated activity. Remarkably, the decreased action potential temporal precision could be restored in mutants by treatment with either the NMDAR antagonist (2R)-amino-5-phosphonovaleric acid or the NMDAR 2B subunit-specific antagonist Ro 25-6981.
conclusionsThese results link the function of the dyslexia-associated gene Dcdc2 to spike timing through activity of NMDAR.
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.