ArticleNeurochemical research2015
mTOR and Erk1/2 Signaling in the Cerebrospinal Fluid-Contacting Nucleus is Involved in Neuropathic Pain.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- The cerebrospinal fluid-contacting nucleus CGRP-RAMP1-PKA signaling pathway mediates trigeminal neuralgia and its mechanism.The Korean journal of pain · 2026Article
- Unraveling the Disease Mechanisms of Neuropathic Pain Through Constructing miRNA-mRNA Networks Based on a Rat Model.Brain and behavior · 2025Article
- Fibroblast growth factor 3 contributes to neuropathic pain through Akt/mTOR signaling in mouse primary sensory neurons.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- The mTOR inhibitor rapamycin suppresses trigeminal neuropathic pain and p-MKK4/p-p38 mitogen-activated protein kinase-mediated microglial activation in the trigeminal nucleus caudalis of mice with infraorbital nerve injury.Frontiers in molecular neuroscience · 2023Article
- PI3K/AKT/mTOR signalling inhibitor chrysophanol ameliorates neurobehavioural and neurochemical defects in propionic acid-induced experimental model of autism in adult rats.Metabolic brain disease · 2022Article
- Activation of Neuroinflammation via mTOR Pathway is Disparately Regulated by Differential Target Multiplexed and Traditional Low-Rate Spinal Cord Stimulation in a Neuropathic Pain Model.Journal of pain research · 2022Article
- The Neural Stem Cell Properties of PKD2L1Frontiers in cellular neuroscience · 2021Article
- Identification of Biomarkers Related to Neuropathic Pain Induced by Peripheral Nerve Injury.Journal of molecular neuroscience : MN · 2019Article
- Suberoylanilide Hydroxamic Acid Triggers Autophagy by Influencing the mTOR Pathway in the Spinal Dorsal Horn in a Rat Neuropathic Pain Model.Neurochemical research · 2019Article
- Stereotaxic Coordinates and Morphological Characterization of a Unique Nucleus (CSF-Contacting Nucleus) in Rat.Frontiers in neuroanatomy · 2019Article
- The Establishment of a CSF-Contacting Nucleus "Knockout" Model Animal.Frontiers in neuroanatomy · 2018Article
- Cerebrospinal fluid-contacting nucleus mediates nociception via release of fractalkine.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Hyperbaric oxygen treatment attenuates neuropathic pain by elevating autophagy flux via inhibiting mTOR pathway.American journal of translational research · 2017Article
- Inhibition of Mammalian Target of Rapamycin (mTOR) Signaling in the Insular Cortex Alleviates Neuropathic Pain after Peripheral Nerve Injury.Frontiers in molecular neuroscience · 2017Article
- Chronic persistent post-surgical pain following staging laparotomy for carcinoma of ovary and its relationship to signal transduction genes.The Korean journal of pain · 2016Article
- Role of the RVM in Descending Pain Regulation Originating from the Cerebrospinal Fluid-Contacting Nucleus.Neurochemical research · 2016Article
- The Involvement of Mutual Inhibition of ERK and mTOR in PLCγ1-Mediated MMP-13 Expression in Human Osteoarthritis Chondrocytes.International journal of molecular sciences · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cerebrospinal fluid-contacting nucleus (CSF-CN) has been demonstrated to be involved in neuropathic pain, but the underlying molecular mechanisms remain unclear. Previous work has shown that mTOR and ERK1/2 are important signaling pathways regulating neuropathic pain. However, studies on the interactions between these major pathways in neuropathic pain are very rare. Therefore, the purpose of this study is to determine whether mTOR and ERK1/2 exist in the CSF-CN and elucidate their alterations in neuropathic pain, especially, the crosstalk between them. Our results showed that mTOR and ERK1/2 were distributed in the CSF-CN, and their expression levels were increased in chronic constriction injury (CCI)-induced neuropathic pain. Furthermore, the injection of both the mTOR antagonist rapamycin and the ERK1/2 antagonist U0126 into the lateral ventricle of the brain attenuated CCI-induced neuropathic pain. Inhibition of the ERK1/2 pathway had little impact on mTOR signaling, but inhibition of the mTOR pathway significantly increased ERK/2 signaling. The coadministration of rapamycin and U0126 inhibited the rapamycin-induced upregulation of ERK, and had a greater effect on pain behaviors than did the single-drug administrations. These data extend our understanding of the relationship between mTOR and ERK in the supraspinal site and demonstrate that the CSF-CN participates in neuropathic pain via the regulation of mTOR and ERK1/2.
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