Traditional Chinese medicine (TCM) have unique efficacy and advantages for treating diseases of central nervous system. In recent years, some researches focused on neural stem cells and neurogenesis. The researches about TCM for influencing neural stem cells biological characteristics and common neurological diseases were reviewed.

Adenosine is an important signaling molecule of the central nervous system (CNS). Adenosine typically released in the phosphorylated form(ATP), together with neurotransmitter, both of which are encapsulated in the synaptic vesicles. Once released into the synaptic space, adenosine molecules will bind to their three categories of receptors, namely A1 receptor (A1R), A2 receptor (A2R), A3 receptor (A3R), and therefore start G protein mediated signaling pathways, resulting in various and extensive biological effects. It has been discovered in recent years that adenosine has a certain level of anti-depression effect, although its mechanisms are yet to be elucidated. This review summarized the researches focusing on anti-depression roles of both adenosine and its receptors.

The monosialic acid ganglioside GM1 is rich in brain, which participates in the development process of the nerve system and plays wide neuroprotective roles. This article reviews recent reports about six neuroprotective mechanisms including: activating tyrosine kinase receptor——Trk receptor, modulating Ca 2+ homeostasis in cells, reducing the deposition of A? and its toxic roles in brain, inhibiting the production of reactive oxygen species, enhancing the activity of Na+,K+-ATPase.

?receptors are particularly abundant in the CNS. ? receptors have been shown to exhibit such a wide variety of actions as modulating glutaminergic, dopaminergic and cholinergic neurotransmission. They also play an important role in maintaining cell growth and proliferation, learning and memory. Recent evidence suggests the possible involvement of ? receptors in the pathogenesis of schizophrenia. More researches are expected to supply new targets for treatment and diagnosis.

ObjectiveTo study the effect of XGS Capsule on the femoral head necrosis in mouse and rat. MethodsThe animal model of femoral head necrosis was caused with tretinoin per os. The free locomotive activity, bone density and pathological changed were observed. ResultsIn the model mouse, the free locomotive activity decreased significantly(P<0.01). In the model rat, the density and weight of the bone also decreased(P<0.01). The defects of cartilage, disorders of ossification and dead bone were observed in the femoral head joint. After treatment with XGS Capsule for 5 weeks, these pathological changes significantly improved. Conclusions XGS Capsule was effective in treating the femoral head necrosis.

ObjectiveTo establish a method of isolation and culture of neural stem cells(NSCs). MethodsTissues of ventral midbrain were isolated from a rat embryo,and the NSCs were cultured stimulated with basic fibroblast growth factor(bFGF)in vitro.The cells were identified by immunocytochemistry.ResultsNSCs proliferated into neurosphere in symmetric and non-symmetric cleavage ways,and differentiated into neuron, astroglia and oligodendrosyte. ConclusionsThe method has been established to isolate and culture the neural stem cells.

Oxidative stress and mitochondria disorder are the common mechanism of neurodegenerative disease, such as Alzheimer disease and Parkinson disease. Melatonin (MT) level decreases with aging may be one of the reasons of the increased oxidative stress in aging people. So the neuroprotective effect of MT becomes more attractive in recent years. This paper summarized recent studies on the mechanism of melatonin on degenerative disease, including free radical scavenge, anti-apoptosis, neuroprotective effect, neurotrophic effect, anti-amyloid neurotoxicity, regulation of inflammatory reaction and cytoskeletal protein etc.

Objective To explore the effect of α-zearalanol (α-ZAL) on β-amyloid (Aβ) induced mice and the mechanism. Methods The model was induced by intracerebroventricular injection of Aβ25-35. The mice were divided randomly into sham group, model group, estradiol benzoate (EB) group (Aβ+EB) as a positive control and α-ZAL (Aβ+α-ZAL) group. Morris water maze was used to evaluate the learning and memory ability. The levels of antioxidant enzymes and nitric oxide system in the brain tissue were detected with spectrophotometric and sotopic method. Results The escape latency was longer in the model group than in the control group (P<0.01), and was shorter in the EB group and α-ZAL group than in the model group (P<0.05). Compared with the control group, the level of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) decreased, and the level of malonaldehyde (MDA), constitutive nitric oxide synthase (cNOS), inducible nitrous oxide synthesis (iNOS), and nitric oxide (NO) increased in the model group (P<0.05); compared with the model group, the level of SOD and GSH-Px increased, and the level of MDA, cNOS, iNOS and NO decreased in the EB group and α-ZAL group (P<0.05), except the level of SOD and cNOS in hippocampus in α-ZAL group (P>0.05). There was no significant difference between EB group and α-ZAL group (P>0.05). Conclusion α-ZAL could improve the cognitive behavior in Aβ25- 35 induced mice by increasing the antioxidant activities and decreasing the lipid peroxidation.

There are a large amount of neural stem cells in the olfactory system which have an active proliferation, ongoing and direc-tional differentiation and migration in order to adapt to the changing environment. The clinical findings showed that the early stages of some neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease all presented dysosmia. In recent years, the relationship be-tween air pollution and dysosmia attracts public concerns. This article introduced some research progresses in this field.

Objective To investigate the effects of NO synthesis inhibition on pain threshold and binding capacity of NMDA receptor of hippocampus in rats. Methods Sixty-six SD rats of both sexes weighing (210 ? 20)g were randomly divided into 11 groups of six. Group I was used for determination of baseline values of pain threshold and binding capacity of NMDA receptor. In the five L-NAME groups (group Ⅱ-Ⅵ) 1% L-NAME in normal saline 50mg?kg-1 was given intraperitoneally (IP) . In the acute experiment pain threshold was determined 15 min (group Ⅱ ) and 30 min (group Ⅲ) after L-NAME IP injection. In the chronic experiment L-NAME 50mg?kg-1 was given IP twice a day for 1 day (group Ⅳ), 4 d (group Ⅴ) and 7 d (group Ⅵ) and pain threshold was measured 12h after last L-NAME administration. Group Ⅶ-Ⅺ served as control groups in which normal saline was given IP instead of L-NAME. Pain threshold was measured by response latencies following CO2 laser stimulation which was delivered to the medial surface of the ear. After determination of pain threshold the animals were decapitated and hippocampus was removed. The binding capacity of NMDA receptor with [3H] MK-801 was determined. Bmax and KD were determined by Scatchard analysis. Results There was no significant difference in pain threshold and binding capacity of NMDA receptor between group Ⅱ ,Ⅲ (acute experiment) and their control groups ( Ⅻ,Ⅷ). In chronic experiment pain threshold significantly increased after 1 and 4 d of L-NAME administration (group Ⅳ and Ⅴ) but return to the baseline value on the 7th day. NMDA receptor binding capacity increased in all three groups of chronic experiment. Bmax was significantly higher than the baseline value on the 4th and 7th day (group Ⅴ and Ⅵ). KD was significantly higher than the baseline value on the 4th day (group Ⅴ) but returned to the baseline on the 7th day (group Ⅵ) . Conclusions In chronic experiment NO synthesis inhibition can increase pain threshold to laser thermal nociceptive stimulation and induce changes in the affinity and density of NMDA receptor.