ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Neuronal pentraxins mediate silent synapse conversion in the developing visual system.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Dissecting the Epigenetic Changes Induced by Non-Antipsychotic Mood Stabilizers on Schizophrenia and Affective Disorders: A Systematic Review.Frontiers in pharmacology · 2020Pooled it
- Mapping the Retina onto the Brain.Cold Spring Harbor perspectives in biology · 2024Review
- Synapse Regulation.Advances in neurobiology · 2024Review
- An interventional study of baicalin on neuronal pentraxin-1, neuronal pentraxin-2, and C-reactive protein in Alzheimer's disease rat model.Translational neuroscience · 2023Article
- Different Synaptic Plasticity After Physiological and Psychological Stress in the Anterior Insular Cortex in an Observational Fear Mouse Model.Frontiers in synaptic neuroscience · 2022Article
- Loss of P2Y12 Has Behavioral Effects in the Adult Mouse.International journal of molecular sciences · 2021Article
- Retinal Ganglion Cell Degeneration in a Rat Magnetic Bead Model of Ocular Hypertensive Glaucoma.Translational vision science & technology · 2021Article
- Overexpression of NPTX2 Promotes Malignant Phenotype of Epithelial Ovarian CarcinomaFrontiers in oncology · 2021Article
- C1QL3 promotes cell-cell adhesion by mediating complex formation between ADGRB3/BAI3 and neuronal pentraxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Sex difference in synaptic plasticity in the anterior cingulate cortex of adult mice.Molecular brain · 2020Article
- Molecular signatures of retinal ganglion cells revealed through single cell profiling.Scientific reports · 2019Article
- Synaptic Elimination in Neurological Disorders.Current neuropharmacology · 2019Review
- Molecular guidance cues in the development of visual pathway.Protein & cell · 2018Review
- Neuronal pentraxin 1: A synaptic-derived plasma biomarker in Alzheimer's disease.Neurobiology of disease · 2018Article
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- Presynaptic Neuronal Pentraxin Receptor Organizes Excitatory and Inhibitory Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Long Noncoding RNA-Directed Epigenetic Regulation of Gene Expression Is Associated With Anxiety-like Behavior in Mice.Biological psychiatry · 2015Article
- Pentraxins coordinate excitatory synapse maturation and circuit integration of parvalbumin interneurons.Neuron · 2015Article
- Parallel age-associated changes in brain and plasma neuronal pentraxin receptor levels in a transgenic APP/PS1 rat model of Alzheimer's disease.Neurobiology of disease · 2015Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal pentraxins (NPs) are hypothesized to play important roles in the recruitment of AMPA receptors (AMPARs) to immature synapses, yet a physiological role for NPs at nascent synapses in vivo has remained elusive. Here we report that the loss of NP1 and NP2 (NP1/2) leads to a dramatic and specific reduction in AMPAR-mediated transmission at developing visual system synapses. In thalamic slices taken from early postnatal mice (<P10) NP1/2 knock-out (KO) neurons displayed severely reduced AMPAR-mediated retinogeniculate transmission. The reduced currents reflected an increased number of silent synapses with no change in quantal amplitude or presynaptic release. These are the first data to demonstrate that NP1/2 are required in vivo for the normal development of AMPAR-mediated transmission. In addition, they suggest a novel role for NP1/2 in silent synapse conversion during a discrete developmental period when visual circuit connections are undergoing eye-specific refinement. After this period, retinogeniculate transmission not only recovered in the knock-outs but became excessive. The enhanced currents were attributable, at least in part, to a deficit in the characteristic elimination of functional inputs that occurs in the developing dLGN. These data indicate that the loss of NP1/2 disrupts several aspects of retinogeniculate development including the initial establishment of AMPAR transmission and the subsequent elimination of inappropriate circuit connections.
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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.