Articles: neuralgia.
-
Neurochemical research · Apr 2015
IL-10 and IL-1β mediate neuropathic-pain like behavior in the ventrolateral orbital cortex.
Previous evidence has shown that the glial cells can be activated by peripheral nerve injury and release both pro-inflammatory and anti-inflammatory cytokines, which play crucial roles in the establishment and maintenance of neuropathic pain. The present study examined the roles of anti-inflammatory cytokine IL-10 and pro-inflammatory IL-1β on allodynia induced by spared nerve injury (SNI) in the ventrolateral orbital cortex (VLO) in the rat. The mechanical paw withdrawal threshold (PWT) was measured using von-Frey filaments. ⋯ Moreover, western blotting results showed expression levels of IL-10 and IL-1β significantly up-regulated in the contralateral VLO of SNI rats as compared with that of sham-operated rats. These results suggest that anti-inflammatory cytokine IL-10 and pro-inflammatory cytokine IL-1β mediate neuropathic-pain like behavior at the cerebral cortex level; IL-10 released from activated glial cells in the VLO can potentially attenuate allodynia while IL-1β released from activated glial cells in the VLO can potentially maintain or facilitate allodynia. These results provide new insights and site for therapy at the cerebral cortex level in neuropathic pain condition.
-
Neural circuits that determine the perception and modulation of pain remain poorly understood. The prefrontal cortex (PFC) provides top-down control of sensory and affective processes. While animal and human imaging studies have shown that the PFC is involved in pain regulation, its exact role in pain states remains incompletely understood. ⋯ PFC activation also reduces the affective symptoms of pain. Furthermore, we show that this pain-relieving function of the PFC is likely mediated by projections to the NAc. Thus, our results support a novel role for corticostriatal circuitry in pain regulation.
-
The α7 nicotinic acetylcholine receptor (nAChR) is a promising drug target for a number of neurological disorders including chronic pain and inflammatory diseases. Since α7 can function as a ligand-gated ion channel, drug development initially focused on ligands that were selective activators of the α7 ion channel. However, the best α7 drugs for chronic pain and inflammation indications may not be ion channel activators but rather "silent agonists", which bind to the receptor but preferentially induce non-conducting states that modulate signal transduction in non-neuronal cells. ⋯ The antinociceptive activity of NS6740 in these models was α7-dependent. In addition, NS6740 administration reversed pain-induced aversion, an important affective component of pain. The time and concentration dependence of the effects were consistent with NS6740 induction of PAM-insensitive non-conducting states, suggesting that signal transduction required for analgesia is accomplished by α7 receptors in that conformation.
-
Although sleep disorder is one of the most serious comorbidities of refractory chronic pain, it is usually assessed only from the patients' subjective point of view. Therefore, we aimed to objectively evaluate the sleep efficiency of patients with chronic pain. ⋯ With the use of an actigraph, improvements in sleep of patients with chronic pain undergoing SCS were demonstrated. One case showing improvement in sleep despite pain palliation may suggest that SCS might have independently affected the sleep system, although further studies are necessary.
-
Models that simulate clinical conditions are needed to gain an understanding of the mechanism involved during spinal cord stimulation (SCS) treatment of chronic neuropathic pain. An animal model has been developed for continuous SCS in which animals that have been injured to develop neuropathic pain behavior were allowed to carry on with regular daily activities while being stimulated for 72 hours. ⋯ A continuous SCS model has been developed. Animals with neuropathic pain behavior that were continuously stimulated showed significant increase in withdrawal thresholds proportional to stimulation time.