Neuroscience letters
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DTNBP1 is a key candidate gene associated with schizophrenia. The expression of its protein product, dysbindin-1, is altered in the brains of schizophrenic patients; however, the physiological functions of dysbindin-1 in the central nervous system are unclear. Several studies have shown that both dysbindin-1 and histone deacetylase 3 (HDAC3) can be phosphorylated by the DNA-dependent protein kinase complex. ⋯ The interaction between dysbindin-1 and HDAC3 occurred in an isoform-specific manner: HDAC3 coupled with dysbindin-1A and -1B, but not -1C. We also found that dysbindin-1B expression was increased in the nucleus in the presence of HDAC3, and, conversely, that the phosphorylation level of HDAC3 increased in the presence of dysbindin-1B. Taken together, these results identify a novel binding partner for dysbindin-1, which may potentially provide a new avenue for research into the neurological mechanisms of schizophrenia.
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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.