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Activation of Double-Stranded RNA –Activated Protein Kinase in the Dorsal Root Ganglia and Spinal Dorsal Horn Regulates Neuropathic Pain Following Peripheral Nerve Injury in Rats
AbstractDouble-stranded RNA (dsRNA) –activated kinase (PKR) is an important component in inflammation and immune dysfunction. However, the role of PKR in neuropathic pain remains unclear. Here, we showed that lumbar 5 spinal nerve ligation (SNL) led to a significant increase in the level of phosphorylated PKR (p-PKR) in both the dor sal root ganglia (DRG) and spinal dorsal horn. Images of double immunofluorescence staining revealed that p-PKR was expressed in myelinated A-fibers, unmyelinated C-fibers, and satellite glial cells in the DRG. In the dorsal horn, p-PKR was located in neuronal cells, astrocytes, and microglia...
Source: Neurotherapeutics - June 2, 2022 Category: Neurology Source Type: research

Blocking the Spinal Fbxo3/CARM1/K + Channel Epigenetic Silencing Pathway as a Strategy for Neuropathic Pain Relief
AbstractMany epigenetic regulators are involved in pain-associated spinal plasticity. Coactivator-associated arginine methyltransferase 1 (CARM1), an epigenetic regulator of histone arginine methylation, is a highly interesting target in neuroplasticity. However, its potential contribution to spinal plasticity –associated neuropathic pain development remains poorly explored. Here, we report that nerve injury decreased the expression of spinal CARM1 and induced allodynia. Moreover, decreasing spinal CARM1 expression by Fbxo3-mediated CARM1 ubiquitination promoted H3R17me2 decrement at the K+ channel promoter, thereby caus...
Source: Neurotherapeutics - January 7, 2021 Category: Neurology Source Type: research

Chronic morphine-mediated upregulation of high mobility group box 1 in the spinal cord contributes to analgesic tolerance and hyperalgesia in rats
We examined whether spinal high mobility group box 1 (HMGB1) is involved in morphine tolerance and its underlying mechanisms by using a model of repeated intrathecal (i.t.) injections of morphine. The results showed that chronic i.t. morphine exposure led to increased expression of HMGB1, Toll-like receptor 4 (TLR4), and receptor for advanced glycation end products (RAGE) and their mRNAs in the dorsal horn. Morphine challenge also promoted HMGB1 expression and release in cultured spinal neurons, but these effects were inhibited by TAK-242, naloxone (antagonists of TLR4), and TLR4 siRNA. Intrathecal coadministration of morp...
Source: Neurotherapeutics - December 25, 2019 Category: Neurology Source Type: research