Skin-derived precursors (SKPs) are derived from mesoblast and can differentiate into smooth muscle cells, adipocytes, and less neuronal phenotypes. This study demonstrates that retinoic acid (RA) improves SKPs exit from self-proliferation to neural differentiation through up-regulating of NeuroD andcell-cycle regulatory protein p21, meanwhile RA also induces p75 neurotrophin receptor (p75NTR) upregulation and apoptosis of SKPs. When treated sequentially with neurotrophin-3 (NT-3) after RA induction, the survival and neural differentiation of SKPs were enhanced significantly, and cell apoptosis induced by RA was decreased. These effects could be reversed by p75NTR inhibitor Pep5 instead of Trk receptor inhibitor K252a. The results indicate that NT-3 improves the neural differentiation of SKPs induced by RA through a p75NTR-dependent signaling pathway

The present study investigated whether morphine can promote regeneration and synaptic reconstruction of the terminals of injured primary afferent fibers in lamina II of the spinal cord in rats following sciatic nerve injury. Fluoride-resistant acid phosphatase (FRAP)- positive terminals in lamina II of the L4 spinal segment after sciatic nerve injury were assessed after treatment with vehicle, morphine, and naloxone plus morphine. Under the electron microscope, types I and II complex terminals of unmyelinated afferent fibers from the dorsal root, simple terminals of interneuronal axons, and terminals of descending axons at lamina II of the L4 spinal segment were documented in the different groups after injury. FRAP-positive terminals in lamina II were depleted after sciatic nerve injury in the vehicle group. Treatment with morphine increased the numbers of FRAP-positive terminals, and this was prevented by naloxone. The present study demonstrates that morphine may promote the regeneration and synaptic reconstruction of the terminals of injured primary unmyelinated afferent fibers in lamina II of spinal cord, by a process mediated by μ-opioid receptors.

Bone marrow mesenchymal stem cells (MSCs) are one of the potential tools fortreatment of the spinal cord injury; however, the survival and differentiation of MSCs in an injuredspinal cord still need to be improved. In the present study, we investigated whether Governor Vesselelectro-acupuncture (EA) could efficiently promote bone marrow mesenchymal stem cells (MSCs)survival and differentiation, axonal regeneration and finally, functional recovery in the transectedspinal cord.

This study investigated whether electro-acupuncture (EA) would improvethe survival and migration of neural stem cells (NSCs) transplanted ininjured spinal cord as well as the potential mechanisms. TlO spinal cordsegments of 50 adult Sprague-Dawley (SD) rats were completely transected,and then NSCs were immediately transplanted into the transected site of theexperimental animals, while control animals were sham operated withouttransplantation. Five days post-operation, electro-acupuncture treatment onGV9 (Zhiyang), GV6 (Jizhong), GV2 (Yaoshu) and GVI (Changqiang)acupoints was applied for 14 days (EA+NSCs 14d) and 30 days (EA+NSCs30d). ELISA and immunohistochemical staining were used to assess thecontent of neurotrophine-3 (NT-3) and the characteristics of transplantedNSCs. We found that the number of transplanted NSCs the survived inEA+NSCs14d group was significantly increased as compared to that of theNSCs30d group (5825.20+819.01vs 4781.40+500.49, P<0.05).19Immunostaining indicated that some transplanted NSCs developed intomicrotubule association protein 2 (MAP2) positive cells and many of themdeveloped into glial fibrillary acidic protein (GFAP) positive cells in theNSCs30d group. Further, the migration length of transplanted NSCs towardcaudal tissue in the injured site was longer in the EA+NSCs30d group thanthat in NSCs30d group (5.98+0.79mm vs 3.96+1.72mm; P<0.05). AlsoNT-3 in injured spinal cord tissue was 23% increased in the EA+NSCs14dgroup. These results suggest that the combination of EA and NSCs improvesthe survival and migration of NSCs in injured spinal cord in rats.

Dendrites and spines undergo dynamic changesin physiological conditions, such as learning and memory, and in pathological conditions, such as Alzheimer's diseaseand epilepsy. Long-term dendritic plasticity has also beenreported after ischemia/hypoxia, which might be compensatoryeffects of surviving neurons for the functional recoveryafter the insults. However, the dendritic changes shortly afterischemia, which might be associated with the pathogenesisof ischemic cell death, remain largely unknown. To reveal themorphological changes of ischemia-vulnerable neurons after ischemia, the present study investigated the alteration ofdendritic arborization of CA1 pyramidal neurons in rats aftertransient cerebral ischemia using intracellular staining techniquein vivo. The general appearance of dendritic arborizationof CA1 neurons within 48 h after ischemia was similar tothat of control neurons. However, a dramatic increase ofdendritic disorientation was observed after ischemia withmany basal dendrites coursed into the territory of apicaldendrites and apical dendrites branched into the region ofbasal dendrites. In addition, a significant increase of apicaldendritic length was found 24 h after ischemia. The increaseof dendritic length after ischemia was mainly due to thedendritic sprouting rather than the extension of individualdendrites, which mainly occurred in the middle segment ofthe apical dendrites. These results reveal a plasticity changein dendritic arborization of CA1 neurons shortly after cerebralischemia.