Studies have shown that functional network connection models can be used to study brain net-work changes in patients with schizophrenia. In this study, we inferred that these models could also be used to explore functional network connectivity changes in stroke patients. We used independent component analysis to find the motor areas of stroke patients, which is a novel way to determine these areas. In this study, we collected functional magnetic resonance imaging datasets from healthy controls and right-handed stroke patients following their ifrst ever stroke. Using independent component analysis, six spatially independent components highly correlat-ed to the experimental paradigm were extracted. Then, the functional network connectivity of both patients and controls was established to observe the differences between them. The results showed that there were 11 connections in the model in the stroke patients, while there were only four connections in the healthy controls. Further analysis found that some damaged connections may be compensated for by new indirect connections or circuits produced after stroke. These connections may have a direct correlation with the degree of stroke rehabilitation. Our ifndings suggest that functional network connectivity in stroke patients is more complex than that in hea-lthy controls, and that there is a compensation loop in the functional network following stroke. This implies that functional network reorganization plays a very important role in the process of rehabilitation after stroke.

In this study, we investigated non-captive four-striped mice (Rhabdomys pumilio) for evidence that adult neurogenesis occurs in the adult brain of animal models in natural environment. Ki-67 (a marker for cell proliferation) and doublecortin (a marker for immature neurons) immunos-taining conifrmed that adult neurogenesis occurs in the active sites of subventricular zone of the lateral ventricle with the migratory stream to the olfactory bulb, and the subgranular zone of the dentate gyrus of the hippocampus. No Ki-67 proliferating cells were observed in the striatum substantia nigra, amygdala, cerebral cortex or dorsal vagal complex. Doublecortin-immunore-active cells were observed in the striatum, third ventricle, cerebral cortex, amygdala, olfactory bulb and along the rostral migratory stream but absent in the substantia nigra and dorsal vagal complex. The potential neurogenic sites in the four-striped mouse species could invariably lead to increased neural plasticity.

MicroRNA-124 (miR-124) is abundantly expressed in neurons in the mammalian central ner-vous system, and plays critical roles in the regulation of gene expression during embryonic neurogenesis and postnatal neural differentiation. However, the expression proifle of miR-124 after spinal cord injury and the underlying regulatory mechanisms are not well understood. In the present study, we examined the expression of miR-124 in mouse brain and spinal cord after spinal cord injury usingin situ hybridization. Furthermore, the expression of miR-124 was examined with quantitative RT-PCR at 1, 3 and 7 days after spinal cord injury. The miR-124 expression in neurons at the site of injury was evaluated by in situ hybridization combined with NeuN immunohistochemical staining. The miR-124 was mainly expressed in neurons through-out the brain and spinal cord. The expression of miR-124 in neurons significantly decreased within 7 days after spinal cord injury. Some of the neurons in the peri-lesion area were NeuN+/miR-124?. Moreover, the neurons distal to the peri-lesion site were NeuN+/miR-124+. These ifndings indicate that miR-124 expression in neurons is reduced after spinal cord injury, and may relfect the severity of spinal cord injury.

Accumulating evidence suggests that the nucleus accumbens, which is involved in mechanisms of reward and addiction, plays a role in the pathogenesis of depression and in the action of anti-depressants. In the current study, intraperitoneal injection of nomifensine, a dopamine reuptake inhibitor, decreased depression-like behaviors in the Wistar Kyoto rat model of depression in the sucrose-preference and forced swim tests. Nomifensine also reduced membrane excitability in medium spiny neurons in the core of the nucleus accumbens in the childhood Wistar Kyoto rats as evaluated by electrophysiological recording. In addition, the expression of dopamine D2-like receptor mRNA was downregulated in the nucleus accumbens, striatum and hippocampus of nomifensine-treated childhood Wistar Kyoto rats. These experimental ifndings indicate that impaired inhibition of medium spiny neurons, mediated by dopamine D2-like receptors, may be involved in the formation of depression-like behavior in childhood Wistar Kyoto rats, and that nomifensine can alleviate depressive behaviors by reducing medium spiny neuron membrane excitability.

Virtual reality is a new technology that simulates a three-dimensional virtual world on a com-puter and enables the generation of visual, audio, and haptic feedback for the full immersion of users. Users can interact with and observe objects in three-dimensional visual space without limitation. At present, virtual reality training has been widely used in rehabilitation therapy for balance dysfunction. This paper summarizes related articles and other articles suggesting that virtual reality training can improve balance dysfunction in patients after neurological diseases. When patients perform virtual reality training, the prefrontal, parietal cortical areas and other motor cortical networks are activated. These activations may be involved in the reconstruction of neurons in the cerebral cortex. Growing evidence from clinical studies reveals that virtual reality training improves the neurological function of patients with spinal cord injury, cerebral palsy and other neurological impairments. These ifndings suggest that virtual reality training can acti-vate the cerebral cortex and improve the spatial orientation capacity of patients, thus facilitating the cortex to control balance and increase motion function.

The transplantation of artificial blood vessels with<6 mm inner diameter as substitutes for human arterioles or veins has not achieved satisfactory results. Umbilical vein has been substituted for ar-tery in vascular transplantation, but it remains unclear whether the stress relaxation and creep tween these vessels are consistent. In this study, we used the fetal umbilical vein and middle cere-bral artery from adult male cadavers to make specimens 15 mm in length, 0.196-0.268 mm in nica media thickness, and 2.82-2.96 mm in outer diameter. The results demonstrated that the stress decrease at 7 200 seconds was similar between the middle cerebral artery and fetal umbilical vein specimens, regardless of initial stress of 18.7 kPa or 22.5 kPa. However, the strain increase at 7 200 seconds of fetal umbilical veins was larger than that of middle cerebral arteries. Moreover, the stress relaxation experiment showed that the stress decrease at 7 200 seconds of the fetal umbilical vein and middle cerebral artery specimens under 22.5 kPa initial stress was less than the decrease in these specimens under 18.7 kPa initial stress. These results indicate that the fetal umbilical vein has appropriate stress relaxation and creep properties for transplantation. These properties are advantageous for vascular reconstruction, indicating that the fetal umbilical vein can be transplanted to repair middle cerebral artery injury.

缺血性脑卒中后神经可塑性与运动功能恢复研究进展

卒中是导致死亡的第1位原因,也是导致成人致残的首要原因[1].在既往报道的大量缺血性脑卒中病例中,仅少数患者完全恢复,大多数患者残留有不同程度的永久性缺陷[2].然而,尽管卒中造成的功能损害很严重,但由于受损神经的重塑及相应部位的功能重组,受损功能仍能得以不断的恢复.本综述旨在介绍缺血性脑卒中后神经可塑性与运动功能的恢复的关系及其可能机制,为康复治疗提供有价值的资料.