Neuroscience letters
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Neuroscience letters · Oct 2014
Spinal cord stimulation exerts analgesia effects in chronic constriction injury rats via suppression of the TLR4/NF-κB pathway.
Spinal cord stimulation (SCS) is an established method for treating chronic neuropathic pain. However, the mechanisms underlying the pain relieving effect of SCS on neuropathic pain remain unclear. Evidence shows that the toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB signal transduction pathway plays a key role in chronic neuropathic pain. ⋯ Compared with the control group, the CCI rats displayed a significantly decreased MWT. After SCS for 3 days, the expression of TLR4/NF-κB and the levels of interleukin(IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in the spinal cord were lower in the SCS group compared to those in the CCI and sham spinal cord stimulation (S-SCS) groups. These results indicate that SCS could effectively attenuate neuropathic pain in CCI rats by inhibiting the activation of the TLR4/NF-κB signaling pathway and by inhibiting the up-regulation of pro-inflammatory cytokines in the spinal cord.
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Neuroscience letters · Oct 2014
The dorsolateral prefrontal network is involved in pain perception in knee osteoarthritis patients.
Functional MRI (fMRI) studies have been used to investigate how the brain processes noxious stimuli in osteoarthritis (OA) and to identify the cortical location of pain perception. However, no consensus has been reached regarding brain activity associated with pain-induced conditions in OA patients. We examined cerebral responses using intra-epidermal electrical stimulation of the . knee in knee OA patients. ⋯ We used fMRI to identify differences in response between healthy subjects and knee OA patients and explored the modulating cortico-subcortical and cortico-cortical pathways using psychophysiological interaction (PPI) analysis. Our results show that chronic pain results in a different brain activation profile in the DLPFC and the pain matrix in knee OA patients. Abnormal brain connectivity between the DLPFC and the pain matrix is induced by chronic pain in knee OA patients.
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Neuroscience letters · Oct 2014
Endogenous neuropeptide S tone influences sleep-wake rhythm in rats.
Neuropeptide S (NPS) is an endogenous peptide that exerts wakefulness promoting, analgesic, and anxiolytic effects when administered exogenously. However, it remains to be determined if endogenous NPS tone is involved in the control of the diurnal sleep-wake cycle, or spontanous behavior. In this study, we examined the effects of the NPS receptor antagonist [D-Cys((t)Bu)(5)]NPS (2 and 20 nmol, icv) on physiological sleep and spontaneous locomotor behavior. ⋯ There was no statistically significant difference in time spent in REMS. There were no behavioral changes including abnormal gross motor behavior in response to [D-Cys((t)Bu)(5)]NPS administration. Collectively these data suggest an involvement of the endogenous NPS/NPS receptor system in physiological sleep architecture.
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Neuroscience letters · Sep 2014
Docosahexaenoic acid intake ameliorates ketamine-induced impairment of spatial cognition and learning ability in ICR mice.
Several studies have reported the ketamine-induced cognitive impairment. Docosahexaenoic acid (DHA) supplementation improves cognitive function in human infants and protects against learning impairment in patients with Alzheimer's disease (AD). In this study, we investigated the effect of DHA on ketamine-induced impairment of spatial cognition and learning ability in Institute of Cancer Research (ICR) mice. ⋯ The results showed that intraperitoneal injection of ketamine (30mg/kg, twice per day) for 4 weeks led to the decline of spatial cognitive ability in mice, and 420mg/(kgd) DHA supplementation for 6 weeks improved ketamine-induced spatial cognitive impairment to a certain extent. The up-regulation of GABA levels in the hippocampus and prefrontal cortex was related to the improvement in spatial learning. Our results suggested that DHA supplementation would be a promising intervention to improve ketamine-induced spatial memory and cognitive dysfunction, and this effect of DHA might be correlated with the up-regulation of GABA levels.
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Neuroscience letters · Sep 2014
Disrupted MEK/ERK signaling in the medial orbital cortex and dorsal endopiriform nuclei of the prefrontal cortex in a chronic restraint stress mouse model of depression.
Depression is one of the most prevalent mental illnesses, and causes a constant feeling of sadness and lose of interest, which often leads to suicide. Evidence suggests that depression is associated with aberrant MEK/ERK signaling. However, studies on MEK/ERK signaling in depression have only been done in a few brain regions, such as the hippocampus and mesolimbic reward pathways. ⋯ This depressive behavior was ameliorated by imipramine. The behavioral changes well corresponded to a decrease in MEK/ERK immunoreactivity in the medial orbital (MO) cortex and dorsal endopiriform nuclei (DEn), which was averted by imipramine, but not in cingulate, prelimbic, infralimbic, and motor cortex. These results suggest that MEK/ERK signaling is disrupted in the DEn and MO subregions of the prefrontal cortex in the depressive phenotype, and that blocking a decrease in activated MEK/ERK is inherent to the antidepressant imipramine response.