Brain research
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Exposure to social stressors can cause profound changes in an individual's physiology and behavior. In Syrian hamsters, even a single social defeat results in conditioned defeat, which includes an abolishment of territorial aggression and the emergence of high levels of submissive behavior. The purpose of the current study was to determine whether the lateral septum (LS) is a component of the putative neural circuit underlying conditioned defeat. ⋯ Experiment 3 examined whether the effects of muscimol on aggression were dependent on prior social defeat. Non-defeated animals receiving muscimol infusions prior to testing with a non-aggressive intruder displayed significantly more aggression than did hamsters receiving control injections. Thus, these data suggest that the activation of GABA(A) receptors in the LS increases aggression regardless of whether or not a hamster has previously experienced social defeat.
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Fragile X Syndrome (FXS) is the most common inherited form of intellectual disability, with behaviors characteristic of autism. Symptoms include abnormal social behavior, repetitive behavior, communication disorders, and seizures. Many symptoms of FXS have been replicated in the Fmr1 knockout (KO) mice. ⋯ Calling rate increased and was similar to WT controls in adult Fmr1 KO mice treated with minocycline for four weeks from birth (P0-P28). All acoustic properties measured were similar in treated and untreated WT control mice indicating minocycline effects were specific to vocalizations in the Fmr1 KO mice. These data suggest that mating-related USVs are robust and relevant biomarkers of FXS, and that minocycline treatment is a promising avenue for treatment of FXS symptoms.
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Nogo-A, oligodendrocyte myelin glycoprotein (OMgp) and myelin-associated glycoprotein (MAG) are known as myelin-associated proteins that inhibit axon growth by binding a common receptor, the Nogo66 receptor (NgR). In the CNS, Nogo-A, OMgp and MAG are predominantly expressed by oligodendrocytes. As our previous study revealed that oligodendrocyte progenitor cells (OPCs) did not inhibit neurite outgrowth, it is not clear whether these myelin-associated proteins are expressed in OPCs, and what functions they perform if they are expressed in OPCs. ⋯ These results suggested that under proliferation environment, the functions of Nogo-A, OMgp and NgR expressed in OPCs might be to control the length of processes, thus maintaining the morphology of OPCs. While in differentiation environment, the functions of Nogo-A, OMgp and NgR expressed in OPCs turned to promote the differentiation of OPCs, thus facilitating the maturation of oligodendrocytes. And NgR, as the common receptor for Nogo-A and OMgp, might be the main molecule that mediated these functions in OPCs.
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Ischemic postconditioning (IPost) has been shown to attenuate cerebral ischemia-reperfusion injury. However, the mechanism remains elusive. Because opening of the mitochondrial permeability transition pore (MPTP) is a crucial determinant of cell death after ischemia-reperfusion, we hypothesized that the neuroprotective effect of IPost may be associated with inhibition of MPTP opening. ⋯ Brain mitochondria were isolated after reperfusion and MPTP activity was evaluated. IPost or CsA treatment significantly improved NDS and reduced infarction volume, while Atr reversed the neuroprotective effects of IPost, and attenuated the decrease in mitochondrial swelling induced by IPost or CsA. Thus, inhibiting MPTP opening may play a crucial role in the neuroprotective effects of IPost, which may have potential clinical value against cerebral ischemia-reperfusion injury.
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Triptolide is a potent immunosuppressive drug capable of inhibiting T cell activation and proliferation. Recent studies show that T cells play an important role in neuropathic pain following nerve injury in rats. In this study, we investigated the effect of triptolide on T cell activation and development of neuropathic pain. ⋯ In the present study, we demonstrated the suppressive effect of triptolide on the development of neuropathic pain. Therefore, triptolide could be a promising immunosuppressive agent in the treatment of neuropathic pain. Further studies are required to examine the safety of intrathecal triptolide for clinical application.