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Stromal cell-derived factor-1 and its receptor CXCR4 are essential regulators of the neurogenesis that occurs in the adult hippocampal dentate gyrus. However, the effects of CXCR7, a new atypical receptor of stromal cell-derived factor-1, on hippocampal neurogenesis after a stroke remain largely unknown. Our study is the first to investigate the effect of a CXCR7-neutralizing antibody on neurogenesis in the dentate gyrus and the associated recovery of cognitive function of rats in the chronic stage of cerebral ischemia. The rats were randomly divided into sham, sham + anti-CXCR7, ischemia and ischemia + anti-CXCR7 groups. Endothelin-1 was injected in the ipsilateral motor cortex and striatum to induce focal cerebral ischemia. Sham group rats were injected with saline instead of endothelin-1 via intracranial injection. Both sham and ischemic rats were treated with intraventricular infusions of CXCR7-neutralizing antibodies for 6 days 1 week after surgery. Immunofluorescence staining with doublecortin, a marker for neuronal precursors, was performed to assess the neurogenesis in the dentate gyrus. We found that anti-CXCR7 antibody infusion enhanced the proliferation and dendritic development of doublecortin-labeled cells in the dentate gyrus in both ischemic and sham-operated rats. Spatial learning and memory functions were assessed by Morris water maze tests 30-32 days after ischemia. CXCR7-neutralizing antibody treatment significantly reduced the escape latency of the spatial navigation trial and increased the time spent in the target quadrant of spatial probe trial in animals that received ischemic insult, but not in sham operated rats. These results suggest that CXCR7-neutralizing antibody enhances the neurogenesis in the dentate gyrus and improves the cognitive function after cerebral ischemia in rats. All animal experimental protocols and procedures were approved by the Institutional Animal Care and Use Committee of China Medical University (CMU16089R) on December 8, 2016., Competing Interests: None

Brain plasticity is very sensitive to the environment. Certain neurotrophic factors and neurotransmitter receptors, including brain-derived neurotrophic factor (BDNF), cyclic adenosine monophosphate response element‑binding protein (CREB), stromal cell‑derived factor‑1 (SDF‑1) and its specific receptor, C-X-C motif chemokine receptor 4 (CXCR4), are important in neurogenesis in adult animals. In the present study, the effects of environmental enrichment (EE) on neurogenesis in the dentate gyrus (DG) and subventricular zone (SVZ), and the protein expression levels of BDNF, CREB, SDF‑1 and CXCR4 were investigated. Adult rats were randomly assigned as controls or underwent EE for 30 days. Subsequently, immunofluorescence staining was used to analyze cell proliferation in the DG and SVZ, and the differentiation and survival of newly‑formed cells in the hippocampus. The protein expression levels of BDNF, phosphorylated CREB (pCREB), protein kinase A catalytic subunit α, SDF‑1 and CXCR4 in the hippocampus were assayed by western blotting. Cognitive function was assessed in a Morris water maze. EE improved cognitive function, and increased the proliferation, differentiation and survival of newly‑formed neurons in the DG of adult rats; however, EE did not activate neurogenesis in the SVZ. Furthermore, EE enhanced the protein expression levels of BDNF, pCREB, SDF-1 and CXCR4 in the hippocampus. These results provide a theoretical basis to explain the beneficial effects of EE on healthy, adult rats.

Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 µg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.

Objectives: Diabetes with cerebral infarction is a common disease that severely impacts health. This study investigated the effect of procyanidin (PC) on the expression of signal transducers and activators of transcription (STAT1) in type 2 diabetes mellitus SD rats with focal cerebral ischemia. We then explored the protective mechanisms of PC in type 2 diabetes mellitus SD rats with focal cerebral ischemia, to provide theory evidence for its clinical application., Methods: We set up a type 2 diabetes mellitus-MCAO model, evaluated neurological function, and used immunohistochemistry methods to measure the activity of STAT1., Results: The brain expression of STAT1 in rats of the sham-operation group was low, but more STAT1 positive cells were found in normal rats with ischemia and in rats with both type 2 diabetes and ischemia when groups were compared with the sham-operation group (p<0.01). Compared with rats that had type 2 diabetes and ischemia, the numbers of STAT1 positive cells after low, medium and high-doses of PC were all decreased (p<0.01), whereby the mid and high-dose groups showed a more substantial decrease (p<0.01) and with no variance between the two groups (p>0.05)., Conclusions: These results indicate that PC has a neuroprotective effect on type 2 diabetes mellitus-MCAO; this may be through decreasing the expression of STAT1, which influences the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway that may inhibit apoptosis to relieve neurological impairment.

A case of a 61-year-old woman with hemichorea associated with nonketotic hyperglycemia is reported. The typical presentation of this disease is nonketotic hyperglycemia, hemichorea, hyper-intense signal on T1-weighted magnetic resonance imaging (MRI) and high-density on computed tomography (CT) in the contralateral striatum. With good glycemic control, the clinical symptoms disappeared.

Aim: To study the expression of leptin receptor (OB-R) and neuronal damage following focal ischemia/reperfusion in rats., Methods: 20 adult male Wistar rats were divided into four groups randomly: sham-operated 24 h,72 h control group and ischemic/reperfusion 24 h, 72 h experiment group. Focal ischemia/reperfusion model was made with MCAO. Immunohistochemistry and immunoelectron microscope were used to observe the expression of OB-R of the cortex and neuronal damage., Results: The positive cells of OB-R were found in pyramidal cells of the parietal cortex, choroid plexus and blood vessel endothelium. Compared with sham-operated group, significant reduction of OB-R positive cells in the pyramidal cells was observed in the ischemia/reperfusion rats 24 hours after cerebral ischemia (P < 0.05). The positive cells of OB-R of sham-operated 72 h group reduced further (P < 0.01). Histochemistry and electron microscope showed neuronal damage in the core area of cerebral ischemia in the late period was more obvious than in the early period., Conclusion: The early and delayed ischemia/reperfusion neuronal damage were accompanied with reduction of OB-R expression. Thus, it is worth to study the effect of OB-R in cerebral ischemia.