ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
p38α and p38β mitogen-activated protein kinases determine cholinergic transdifferentiation of sympathetic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- Preclinical and randomized clinical evaluation of the p38α kinase inhibitor neflamapimod for basal forebrain cholinergic degeneration.Nature communications · 2022Trial
- p38α Mitogen-Activated Protein Kinase-An Emerging Drug Target for the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2024Review
- A cholinergic neuroskeletal interface promotes bone formation during postnatal growth and exercise.Cell stem cell · 2022Article
- Impact of environmental toxicants on p38- and ERK-MAPK signaling pathways in the central nervous system.Neurotoxicology · 2021Review
- SATB2-LEMD2 interaction links nuclear shape plasticity to regulation of cognition-related genes.The EMBO journal · 2021Article
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Ciliary neurotrophic factor signaling in the rat orbitofrontal cortex ameliorates stress-induced deficits in reversal learning.Neuropharmacology · 2019Article
- Genes encoding SATB2-interacting proteins in adult cerebral cortex contribute to human cognitive ability.PLoS genetics · 2019Article
- Neuroregeneration in Parkinson's Disease: From Proteins to Small Molecules.Current neuropharmacology · 2019Review
- Distribution and Neurochemistry of the Porcine Ileocaecal Valve Projecting Sensory Neurons in the Dorsal Root Ganglia and the Influence of Lipopolysaccharide from Different Serotypes ofInternational journal of molecular sciences · 2018Article
- Satb2 determines miRNA expression and long-term memory in the adult central nervous system.eLife · 2016Article
- Crosstalk among electrical activity, trophic factors and morphogenetic proteins in the regulation of neurotransmitter phenotype specification.Journal of chemical neuroanatomy · 2016Review
- The MAPK and PI3K pathways mediate CNTF-induced neuronal survival and process outgrowth in hypothalamic organotypic cultures.Journal of cell communication and signaling · 2015Article
- Satb2-independent acquisition of the cholinergic sudomotor phenotype in rodents.Cellular and molecular neurobiology · 2015Article
- Deletion of interleukin-6 signal transducer gp130 in small sensory neurons attenuates mechanonociception and down-regulates TRPA1 expression.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Dynamic regulation of neurotransmitter specification: relevance to nervous system homeostasis.Neuropharmacology · 2014Review
- Tlx3 controls cholinergic transmitter and Peptide phenotypes in a subset of prenatal sympathetic neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Although the p38 mitogen-activated protein kinases are active in many neuronal populations in the peripheral and central nervous systems, little is known about the physiological functions of p38 in postmitotic neurons. We report that p38 activity determines in vitro and in vivo the switch from noradrenergic to cholinergic neurotransmission that occurs in sympathetic neurons on exposure to the neuropoietic cytokines CNTF and LIF. This transdifferentiation serves as a model for the plastic mechanisms that enable mature neurons to change some of their central functions without passing through the cell cycle. We demonstrate that in postmitotic neurons, p38 and STAT pathways are concurrently activated by neuropoietic cytokine treatment for at least 12 h overlapping with changes in neurotransmitter marker gene expression. Inhibition of p38 blocks the upregulation of the nuclear matrix protein Satb2 and of cholinergic markers by CNTF without affecting STAT3 phosphorylation. Conversely, overexpression of p38α or β in the absence of cytokines stimulates cholinergic marker expression. The neurotransmitter switch in vitro is impaired in neurons isolated from p38β(-/-) mice. Consistent with these in vitro results, a substantial loss of cells expressing cholinergic properties is observed in vivo in the stellate ganglion of mature mice deficient in the p38β isoform.
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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.