Selective astrocyte (α-aminoadipate) and microglia (minocycline) inhibitors were injected i.t. to determine the contribution of these cells to hyperalgesia and paw edema.The effects of i.t. treatments with glial and NFκB (PDTC) inhibitors on spinal glial activation, TNF-α, IL-1β, CX<sub>3</sub>CR1 and CX<sub>3</sub>CL1 mRNA expression, and NFκB activation were also evaluated.
In addition to arachidonic acid, COX-2 oxidizes the endocannabinoid 2-arachidonoylglycerol (2-AG) to produce prostaglandin E<sub>2</sub> (PGE<sub>2</sub>)-glycerol (PGE<sub>2</sub>-G); PGE<sub>2</sub>-G is known to produce hyperalgesia.
The aim of this study is the contribution of TRPV1 to the surface expression of <i>N</i>-methyl-d-aspartate (NMDA) receptors in remifentanil-induced postoperative hyperalgesia.
Selective pharmacological blockade of TRPA1 or TRPV1 showed that TRPA1 is crucially involved in MG-induced chemical pain sensation and heat hyperalgesia.
Selective astrocyte (α-aminoadipate) and microglia (minocycline) inhibitors were injected i.t. to determine the contribution of these cells to hyperalgesia and paw edema.The effects of i.t. treatments with glial and NFκB (PDTC) inhibitors on spinal glial activation, TNF-α, IL-1β, CX<sub>3</sub>CR1 and CX<sub>3</sub>CL1 mRNA expression, and NFκB activation were also evaluated.
By precisely removing a unique PKC phosphorylation site (TRPV1 S801) in mice through CRISPR/Cas9 editing, we provide <i>in vivo</i> evidence for a highly specific inhibition that leaves basal TRPV1 function intact, yet alleviates some forms of hyperalgesia.
In vivo, local administration of TRPV1 antagonists into the lateral habenula attenuated hyperalgesia, anxiety, and relapse-like drinking in rats who chronically consumed alcohol.The data suggest that enhanced TRPV1 channel function during withdrawal may contribute to aberrant behavior that promotes relapse alcohol consumption.
TRPV1 contributes to peripheral sensitization and hyperalgesia, in part, <i>via</i> triggering the release of proinflammatory peptides, such as calcitonin gene-related peptide (CGRP), both locally and at the dorsal horn of the spinal cord.
These results suggest that minocycline provides protection against neonatal systemic LPS exposure-induced enhanced pain sensitivity (allodynia and hyperalgesia), and that the protective effects may be associated with its ability to attenuate LPS-induced microglia activation, and the levels of IL-1β, COX-2, and PGE2 in the spinal cord of neonatal rats.
Pressure stimulation, contact heat stimulation, hyperalgesia (pinprick stimulation) and allodynia (brush stimulation) to mechanical stimulation were performed in the area where capsaicin and NGF were injected.
Similarly, NTG injection produced significant hindpaw mechanical allodynia or facial cold allodynia, but not heat hyperalgesia in transient receptor potential type V1 (TRPV1) knockout mice.
The effects of the COX-2 inhibitor, parecoxib (intraperitoneal 10 mg kg<sup>-1</sup>), or the EP-1R antagonist, SC51089 (intraperitoneal 100 μg kg<sup>-1</sup>), on hyperalgesia and spinal PGE2 were examined.
Rats treated with pre-incision LIA and SNB or post-incision LIA had alleviated hyperalgesia and significantly reduced levels of IL-1β, IL-6, and TNF-α compared to the control group.
The present findings indicate that the BDNF and IL-1ß induction within the dorsal horn may be linked to the development of hyperalgesia, and that opioid analgesics and probably inhibitors of glial cell activation can prevent sensitization in the pain pathway at spinal level.
Intraplantar injection of NGF<sup>R100W</sup> into adult rats induced neither TrkA-mediated thermal nor mechanical acute hyperalgesia, but retained the ability to induce chronic hyperalgesia based on agonism for TrkA signaling.
The aim of the current study was to investigate the effects of those two modalities on pain behavior and the expression of pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6 and tumor necrosis factor-α (TNF-α) in the spinal cord and dorsal root ganglion (DRG) in a rat model of perioperative fentanyl induced hyperalgesia.