Thus, PAP-I mediates the neuron-microglial crosstalk after peripheral nerve injury, and contributes to the maintenance of neuropathic pain.<b>SIGNIFICANCE STATEMENT</b>Neuropathic pain is maladaptive pain condition and the maintaining mechanism is largely unclear.
Noteworthy, 13 hub genes associated with neuropathic pain and nerve regeneration, including Ccl12, Ppp1r15a, Cdkn1a, Atf3, Nts, Dusp1, Ccl7, Csf, Gadd45a, Serpine1, Timp1 were rarely reported in PubMed database, these genes may provide us the new orientation in experimental research and clinical study.
In the dorsal striatum mGluR7 and mGluR8 are located at glutamatergic corticostriatal terminals and their stimulation inhibits pain in pathological conditions such as neuropathic pain.
The expression of chemokines and their receptors, such as CX3CL1/CX3CR1, CCL2/CCR2, CXCL1/CXCR2, CXCL12/CXCR4 and CCL3/CCR5, is altered in the pathological conditions of CIPN, and chemokine receptor antagonists attenuate neuropathic pain behaviour.
However, the mechanism of GluA1-containing AMPA receptor membrane trafficking mediated by SNAP-25 phosphorylation in neuropathic pain deserves further exploration.
The expression levels of MAP3K4 were modulated by the increased miR-183 negatively, which lead to the downregulation of IL-6, IL-1β, and COX-2, and then reduced neuropathic pain progression, respectively.
Many potent iNOS inhibitors with high selectivity over related NOS isoforms, neuronal NOS, and endothelial NOS, have been discovered, and these drugs have shown promise in animal models of endotoxemia, inflammatory and neuropathic pain, arthritis, and other disorders.
We used genetic manipulations and pharmacology to inhibit MNK-eIF4E activity in animals with spared nerve injury, a model of peripheral nerve injury (PNI)-induced neuropathic pain.
Thus, PAP-I mediates the neuron-microglial crosstalk after peripheral nerve injury, and contributes to the maintenance of neuropathic pain.<b>SIGNIFICANCE STATEMENT</b>Neuropathic pain is maladaptive pain condition and the maintaining mechanism is largely unclear.
Meanwhile, nerve injury activated the Wnt1/β-catenin signaling pathway in a quick-onset and sustained manner, and blocking the Wnt1 signaling with a Wnt1 targeting antibody attenuated neuropathic pain.
We observed a differential distribution of C5a and ICAM-1 within sEVs and serum between sham and SNI, indicating changes from local or paracrine to long distance signaling under neuropathic pain.
A functional polymorphism in the ABCB1 transporter predicts pharmacologic response to combination of nortriptyline and morphine in neuropathic pain patients.
In the dorsal striatum mGluR7 and mGluR8 are located at glutamatergic corticostriatal terminals and their stimulation inhibits pain in pathological conditions such as neuropathic pain.
Thus, PAP-I mediates the neuron-microglial crosstalk after peripheral nerve injury, and contributes to the maintenance of neuropathic pain.<b>SIGNIFICANCE STATEMENT</b>Neuropathic pain is maladaptive pain condition and the maintaining mechanism is largely unclear.
Furthermore, the regulatory effect of neurofilament light polypeptide on neuropathic pain was detected using plasmid overexpressing neurofilament light polypeptide.