Neuroscience letters
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Neuroscience letters · Jul 2016
Effects of left primary motor and dorsolateral prefrontal cortex transcranial direct current stimulation on laser-evoked potentials in migraine patients and normal subjects.
Migraine is characterized by an altered cortical excitability. Because transcranial direct current stimulation (tDCS) can change brain activity noninvasively, it is possible to hypothesize its efficacy in modulating pain in migraine. In this study, we compared the effects of tDCS of the left primary motor cortex (M1) and left dorsolateral prefrontal cortex (DLPFC) both on subjective pain and on evoked responses induced by laser stimulation (LEPs). ⋯ We did not find significant acute changes in LEPs parameters and pain perception among subjects who received tDCS of both M1 and DLPFC. After DLPFC tDCS, we observed a significant increase of N2-P2 component habituation in migraine patients while M1 stimulation reduced it. These findings may suggest a modulation of abnormal pain processing induced by DLPFC and M1 anodal tDCS and outline the need for future investigations exploring the possible neuronal plasticity changes supporting the clinical effect on migraine.
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Neuroscience letters · Jul 2016
Up-regulation of CXCL1 and CXCR2 contributes to remifentanil-induced hypernociception via modulating spinal NMDA receptor expression and phosphorylation in rats.
It is commonly known that remifentanil exposure during anesthesia might cause postoperative hyperalgesia and promote nociceptive sensitization, but specific mechanisms remain elusive. Recently, chemokine CXCL1 is considered to be involved in inflammatory and neuropathic pain, simultaneously, CXCL1 might facilitate nociceptive process by increasing of NMDA receptor activity. Several studies have also reported that NMDA receptor activation has been associated with development of remifentanil-induce hypernociception (RIH). However, whether CXCL1 could contribute to RIH in rats remains not understood. ⋯ These findings indicated that up-regulation of CXCL1 and CXCR2 might contribute to RIH via modulating spinal NR2B-containing NMDA receptor expression and phosphorylation in rats.