Neuroscience letters
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Neuroscience letters · Jan 2014
Co-culturing improves the OGD-injured neuron repairing and NSCs differentiation via Notch pathway activation.
Neural stem cell (NSC) transplantation for ischemic stroke is expected to repair the neuronal injury and replace the lost neurons through cell-cell cross talk between injured neurons and the transplanted NSCs. Here, we set up an in vitro co-culturing system of oxygen-glucose deprivation (OGD) injured neurons and NSCs to investigate the neuronal repairing effect and effects on NSCs differentiation. ⋯ When the NSCs were pre-treated with the Notch pathway inhibitor DAPT, the activation of Notch1 was blocked, lower NSCs differentiation was detected and the neurotrophic effect was also abolished. As shown by the novel co-culturing system, the NSCs co-cultured with OGD injured neurons were induced to differentiate through the Notch1 pathway activation; and these induced NSCs showed greater potential to support both the repair of injured neurons and form new neurons.
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Neuroscience letters · Jan 2014
Spinal synaptic scaffolding protein Homer 1b/c regulates CREB phosphorylation and c-fos activation induced by inflammatory pain in rats.
Previous studies have shown that spinal Homer 1b/c plays an important role in the maintenance of chronic inflammatory pain induced by complete Freund's adjuvant (CFA). This study investigated the possible mechanism underlying Homer 1b/c mediating CFA-induced inflammatory pain. Chronic inflammation was induced by CFA injection into the left hind ankle of the rat. ⋯ Immunohistochemistry was conducted to detect the expression of phosphorylated cAMP response element binding protein (pCREB) and Fos protein in the spinal dorsal horn. Intrathecal administration of Homer 1b/c antisense oligonucleotides not only markedly reduced the expression of Homer 1b/c protein, but also attenuated CFA-induced inflammation, spinal CREB phosphorylation, and Fos expression. These results demonstrate for the first time that Homer 1b/c regulates CREB phosphorylation and c-fos activation in the spinal dorsal horn during the maintenance of chronic inflammatory pain, suggesting that Homer 1b/c may be involved in the development of CFA-induced inflammation.
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Evidence suggests that acute and chronic hyperglycemia can cause oxidative stress in the peripheral nervous system which, in turn, can promote the development of diabetic neuropathy. Recent studies have found increased expression of glial fibrillary acidic protein (GFAP) and S100B, both of which are indicators of glial reactivity, in the neural and retinal tissues of diabetic rats. For the first time in the literature, the serum levels of GFAP and S100B were assessed in patients with diabetes to evaluate the potential of these factors to serve as peripheral glial biomarkers of diabetes and to investigate their relationship to diabetic peripheral neuropathy. ⋯ However, we found a statistically significant decrease in S100B serum levels in patients with diabetes compared with control participants (p<0.001). No associations between serum S100B levels and the presence of diabetic peripheral neuropathy or other microvascular complications were observed (p>0.05). The findings of markedly decreased serum levels of S100B may possibly indicate a neuroprotective effect of S100B, whereas GFAP may be of no diagnostic value in human patients with diabetes.
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Neuroscience letters · Jan 2014
Presynaptic inhibitory actions of pregabalin on excitatory transmission in superficial dorsal horn of mouse spinal cord: further characterization of presynaptic mechanisms.
Pregabalin is widely used as an analgesic for the treatment of neuropathic pain. In the present experiments using mouse spinal slices, we recorded electrically evoked glutamatergic excitatory postsynaptic currents (eEPSCs) from superficial dorsal horn neurons. Pregabalin reduced the amplitude of eEPSCs, and increased the paired pulse ratio. ⋯ These results provide further evidence that pregabalin exerts its presynaptic inhibitory action via binding with the α2δ subunit in a state-dependent manner. Furthermore, presynaptic actions of pregabalin were attenuated in knockout mice lacking the protein syntaxin 1A, a component of the synaptic vesicle release machinery, indicating that syntaxin 1A is required for pregabalin to exert its full presynaptic inhibitory action. These observations might suggest that direct and/or indirect interactions with the presynaptic proteins composing the release machinery underlie at least some part of pregabalin's presynaptic actions.