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.

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.

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.

The early characterization of the diazepam-binding sites outside the brain led to their assignment as peripheralbenzodiazepine receptors, or PBRs, to distinguish them from the central benzodiazepine receptor.Although PBR is a widely used and accepted name in the scientific community,recent data regarding the structure and molecular function of this protein increasingly support renaming it to represent more accurately its subcellular role (or roles) and putative tissue-specific function (or functions). Translocator protein (18 ku,TSPO), is proposed as a new name, regardless of the subcellular localization of the protein. This review deals with the pharmacological, structural and molecular characterization of the PBR and its role in the neuropshcopharmacology.

Objective We investigated the effect of Guhong on the capability of brain to resist ischemia.Methods MCAO model was established in SD rats.TTC staining was performed in Guhong group with intraperitoneal injection and routine MCAO model group.Infarction volume was compared.Immunochemistry was performed to observe Caspase 3 expression in peri-infarct cortice of both of the groups.Results Guhong intraperitoneal injection significantly reduced the infarction volume(P﹤0.05).Caspase 3 expression was lower in Guhong group as compared with the model group.Conclusion Guhong may strengthen the capability of brain to resist ischemia.Anti-apoptosisinduced by Guhong may be the one of the underlied mechanisms.

Aim To study Dehydroepiandrosterone (DHEA) and 7-oxo-dehydroepiandrosterone (7-oxo-DHEA) protected hippocampal neurons against neurotoxicity induced by glutamate(Glu). Methods Cell survival rate was analyzed using MTT colorimetry, the change of Ca 2+ levels and the levels of free radical in cultured hippocampal neurons were analyzed by the laser scanning confocal microscope, and cellular GSH level was also analyzed. Results Exposure of cultured rat hippocampal neurons to Glu resulted in accumulation of celluar Ca 2+ and cellular free radical were prevented by DHEA (0.1 ?mol?L -1 )and 7-oxo-DHEA(0.1 ?mol?L -1),and cellular GSH was increased. Conclusion DHEA and 7-oxo-DHEA protected hippocampal neurons against neurotoxicity induced by Glu.

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.

Objective To investigate the effects of isoflurane (Iso) on the water-maze performances in scopolamine (Sco) treated rats.Methods Fifty-five male SD rats weighing 150-200 g were randomly divided into 8 groups :group I control (Con)/1 d ( n = 6); group II Iso/1 d ( n = 7);group III Sco/1 d ( n = 9);group IV Iso + Sco/1 d ( n = 9) ; group V Con/7 d ( n = 6); group VI Iso/7 d ( n = 6); group VII Sco/7 d ( n = 6) and group VIII Iso + Sco/7 d ( n = 6) . In Iso and Iso + Sco groups the animals inhaled 1.5% isoflurane 2 h per day for four consecutive days. The Morris water-maze (MWM) test was performed for 3 consecutive days starting from the first day (group I -IV ) or the 7th day (group V -VII) after the 4 day isoflurane inhalation. Scopolamine 0.8 mg.kg-1 was given ip 20 min before the beginning of the MWM test in Sco and Iso + Sco groups. Results In group I - IV , (1) the latency period and swimming distance were significantly longer in Sco and Iso + Sco group than those in Con and Iso group ( P

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.