ArticleThe Journal of physiology2006
Intracellular sphingosine 1-phosphate mediates the increased excitability produced by nerve growth factor in rat sensory neurons.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 73 citations in OpenAlex.
- Sphingosine-1-phosphate-induced nociceptor excitation and ongoing pain behavior in mice and humans is largely mediated by S1P3 receptor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Trial
- Potential Role of Sphingosine-1-Phosphate and Its Receptors in the Reparative Processes of the Adult Brain.International journal of molecular sciences · 2026Review
- The sphingosine-1-phosphate signaling pathway (sphingosine-1-phosphate and its receptor, sphingosine kinase) and epilepsy.Epilepsia open · 2025Review
- Recent Insight into the Role of Sphingosine-1-Phosphate Lyase in Neurodegeneration.International journal of molecular sciences · 2023Review
- A missense point mutation in nerve growth factor (NGFProgress in neurobiology · 2020Article
- Activation of Sphingosine-1-Phosphate Receptor 1 in the Spinal Cord Produces Mechanohypersensitivity Through the Activation of Inflammasome and IL-1β Pathway.The journal of pain · 2019Article
- Nerve growth factor is expressed and stored in central neurons of adult zebrafish.Journal of anatomy · 2019Article
- Extracellular and intracellular sphingosine-1-phosphate distinctly regulates exocytosis in chromaffin cells.Journal of neurochemistry · 2019Article
- Uncoupling neurotrophic function from nociception of nerve growth factor: what can be learned from a rare human disease?Neural regeneration research · 2019Review
- Metformin protects against sevoflurane-induced neuronal apoptosis through the S1P1 and ERK signaling pathways.Experimental and therapeutic medicine · 2019Article
- CSF levels of apolipoprotein C1 and autotaxin found to associate with neuropathic pain and fibromyalgia.Journal of pain research · 2019Article
- S1PR3 Mediates Itch and Pain via Distinct TRP Channel-Dependent Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Swedish Nerve Growth Factor Mutation (NGFThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Identification of Chloride Channels CLCN3 and CLCN5 Mediating the Excitatory ClFrontiers in molecular neuroscience · 2018Article
- The sphingosine-1-phosphate receptor: A novel therapeutic target for multiple sclerosis and other autoimmune diseases.Clinical immunology (Orlando, Fla.) · 2017Review
- The TrkA receptor mediates experimental thermal hyperalgesia produced by nerve growth factor: Modulation by the p75 neurotrophin receptor.Neuroscience · 2017Article
- The Direct Effects of Fingolimod in the Central Nervous System: Implications for Relapsing Multiple Sclerosis.CNS drugs · 2016Review
- Sphingosine 1-phosphate signaling pathway in inner ear biology. New therapeutic strategies for hearing loss?Frontiers in aging neuroscience · 2015Review
- Sphingosine 1-phosphate to p38 signaling via S1P1 receptor and Gαi/o evokes augmentation of capsaicin-induced ionic currents in mouse sensory neurons.Molecular pain · 2014Article
- The development and maintenance of paclitaxel-induced neuropathic pain require activation of the sphingosine 1-phosphate receptor subtype 1.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous studies found that nerve growth factor (NGF), via ceramide, enhanced the number of action potentials (APs) evoked by a ramp of depolarizing current in capsaicin-sensitive sensory neurons. Ceramide can be metabolized by ceramidase to sphingosine (Sph), and Sph to sphingosine 1-phosphate (S1P) by sphingosine kinase. It is well established that each of these products of sphingomyelin metabolism can act as intracellular signalling molecules. This raises the question as to whether the enhanced excitability produced by NGF was mediated directly by ceramide or required additional metabolism to Sph and/or S1P. Sph applied externally did not affect the neuronal excitability, whereas internally perfused Sph augmented the number of APs evoked by the depolarizing ramp. Furthermore, internally perfused S1P enhanced the number of evoked APs. This sensitizing action of NGF, ceramide and internally perfused Sph was abolished by dimethylsphingosine (DMS), an inhibitor of sphingosine kinase. In contrast, internally perfused S1P enhanced the number of evoked APs in the presence of DMS. These observations support the idea that the metabolism of ceramide/Sph to S1P is critical for the sphingolipid-induced modulation of excitability. Both internally perfused Sph and S1P inhibited the outward K+ current by 25-35% for the step to +60 mV. The Sph- and S1P-sensitive currents had very similar current-voltage relations, suggesting that they were likely to be the same. In addition, the Sph-induced suppression of the K+ current was blocked by pretreatment with DMS. These findings demonstrate that intracellular S1P derived from ceramide acts as an internal second messenger to regulate membrane excitability; however, the effector system whereby S1P modulates excitability remains undetermined.
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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.