ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Regulation of neuronal excitability through pumilio-dependent control of a sodium channel gene.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 136 citations in OpenAlex.
- Natural noncodingScience advances · 2026Article
- Conflicting adaptations in an inhibitory feedback circuit.The Journal of physiology · 2026Article
- Peripheral modulation of Pumilio in intestinal stem cells and the corpus allatum affects sleep latency in Drosophila.PloS one · 2026Article
- Article
- Ectopic sodium channel expression decreases excitability of Drosophila Kenyon cells.The Journal of physiology · 2025Article
- Regulation of theRNA (New York, N.Y.) · 2024Article
- Characterization of NaLife science alliance · 2024Article
- Motor neurons within a network use cell-type specific feedback mechanisms to constrain relationships among ion channel mRNAs.Journal of neurophysiology · 2023Article
- Homeostatic regulation of neuronal function: importance of degeneracy and pleiotropy.Frontiers in cellular neuroscience · 2023Review
- Targeting firing rate neuronal homeostasis can prevent seizures.Disease models & mechanisms · 2022Article
- Mechanisms Driving the Emergence of Neuronal Hyperexcitability in Fragile X Syndrome.International journal of molecular sciences · 2022Review
- RNA and neuronal function: the importance of post-transcriptional regulation.Oxford open neuroscience · 2022Review
- Homeostatic Regulation of Motoneuron Properties in Development.Advances in neurobiology · 2022Review
- Article
- Aedes aegypti miRNA-33 modulates permethrin induced toxicity by regulating VGSC transcripts.Scientific reports · 2021Article
- Mechanisms underlying homeostatic plasticity in theProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Unique repression domains of Pumilio utilize deadenylation and decapping factors to accelerate destruction of target mRNAs.Nucleic acids research · 2020Article
- Silencing SCAMP1-TV2 Inhibited the Malignant Biological Behaviors of Breast Cancer Cells by Interaction With PUM2 to Facilitate INSM1 mRNA Degradation.Frontiers in oncology · 2020Article
- Functions, mechanisms and regulation of Pumilio/Puf family RNA binding proteins: a comprehensive review.Molecular biology reports · 2020Review
- Pumilio Regulates Sleep Homeostasis in Response to Chronic Sleep Deprivation inFrontiers in neuroscience · 2020Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Dynamic changes in synaptic connectivity and strength, which occur during both embryonic development and learning, have the tendency to destabilize neural circuits. To overcome this, neurons have developed a diversity of homeostatic mechanisms to maintain firing within physiologically defined limits. In this study, we show that activity-dependent control of mRNA for a specific voltage-gated Na+ channel [encoded by paralytic (para)] contributes to the regulation of membrane excitability in Drosophila motoneurons. Quantification of para mRNA, by real-time reverse-transcription PCR, shows that levels are significantly decreased in CNSs in which synaptic excitation is elevated, whereas, conversely, they are significantly increased when synaptic vesicle release is blocked. Quantification of mRNA encoding the translational repressor pumilio (pum) reveals a reciprocal regulation to that seen for para. Pumilio is sufficient to influence para mRNA. Thus, para mRNA is significantly elevated in a loss-of-function allele of pum (pum(bemused)), whereas expression of a full-length pum transgene is sufficient to reduce para mRNA. In the absence of pum, increased synaptic excitation fails to reduce para mRNA, showing that Pum is also necessary for activity-dependent regulation of para mRNA. Analysis of voltage-gated Na+ current (I(Na)) mediated by para in two identified motoneurons (termed aCC and RP2) reveals that removal of pum is sufficient to increase one of two separable I(Na) components (persistent I(Na)), whereas overexpression of a pum transgene is sufficient to suppress both components (transient and persistent). We show, through use of anemone toxin (ATX II), that alteration in persistent I(Na) is sufficient to regulate membrane excitability in these two motoneurons.
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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.