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Distinct Roles and Modulations of Synaptic and Extrasynaptic NMDA Receptors CHU Shi-feng, CHEN Nai-hong Acta Neuropharmacologica 2011, 1 (5): 40-48. Abstract（ 8354） PDF（790KB）（ 4515） N-Methyl-D-Aspartate receptor（NMDA receptor） has been considered as a double-edged sword in central nervous system. On the one hand, it mediates the calcium influx, promotes the synaptic plasticity and improves the neural excitatory. On the other hand, excessive opening of NMDA receptor causes calcium overload in neurons, disturbing the homeostasis and inducing the apoptosis. However, growing number of studies demonstrated that the distinct roles of NMDA receptor do not totally depend on its opening degree, but also on its locations where different signaling pathways are triggered. Synaptic NMDA receptors activate the nuclear calcium signaling pathways to protect the neurons; whereas activation of extrasyanptic NMDA receptor starts the apoptosis or death pathway. The imbalance between the two pathways accounts partially for pathogenesis in neural diseases, such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. In conclusion, the currently available evidence has provided a new clue for the treatment of neurodegenerative disease. Reference|Related Articles|Metrics

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Research Progress on Pharmacologic Actions of Curcumin in Central Nervous System LI Gao-wen, XU Ying, KU Bao-shan, PAN Jian-chun ACTA NEUROPHARMACOLOGICA 2011, 1 (2): 48-57. Abstract（ 6655） PDF（1221KB）（ 4516） Curcumin, an active yellow polyphenol pigment of turmeric, belongs to polyphone compound. Quantities of research have proved its pharmacologic actions in peripheral systems, such as antiatherosclerosis, antineoplasms, antidiabetes; In recent years, people have also found curcumin’s therapeutic effects on some neurodegenerative diseases and affective disorders, such as alzheimer’s, parkinson’s, depression, epilepsy and anxiety. As a powerful antioxidative agent, curcumin can modulate the balance of redox and reduce the formation of responsive oxidative species（ROS）, which results in the neuroprotective effect. In addition to these, the neuroprotective effect of curcumin is involved in regulating signal molecules, such as NF-κB Nrf2 p-MEK,p-ERK,c-fos,APP,BACE1.Curcumin can also affect the BDNF/TrkB-MAPK/PI-3K-CREB pathway to regulate the neuroplasticity, cell vitality and antiapoptosis. This review summarizes the effects and possible mechanism of curcumin on neurodegenerative diseases, cerebral ischemia, traumatic brain injury and affective disorders such as depression and anxiety. Reference|Related Articles|Metrics

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Effects of Chrysophanol Liposomes on Apoptosis of the Hippocampal Neurons in Mice after Cerebral Ischemia and Reperfusion Injury SONG Jin-yan, ZHANG Li, ZHAO Xiao-qian, SONG Zhi-bin ACTA NEUROPHARMACOLOGICA 2011, 1 (2): 7-13. Abstract（ 6310） PDF（1243KB）（ 2701） Objective:To observe the influence of chrysophanol liposomes on apoptosis of hippocampal neurons in mice and to study the protective effects on cerebral ischemia and reperfusion injury and its mechanism. Methods:Cerebral ischemia and reperfusion injury was produced in conscious mice by temporarily obstructing bilateral common carotid arteries. Chrysophanol liposomes（10.0，1.0，0.1 mg· kg -1）was injected intraperitoneally. The effects of chrysophanol liposomes were studied on the neurological function, the pathomorphology of brain tissues and the expression of apoptosisrelated protein caspase-3, Bcl-2 and Bax in hippocampal neuron using immunohistochemistry. Results： Chrysophanol liposomes could increase the expression of Bcl-2, decrease the expression of Bax and caspase-3, improve the neurological function score and decrease the pathological change in chrysophanol liposomes treated animals. The effect of chrysophanol liposomes was most obviously in group 10.0 mg· kg -1（ P<0.05）. Conclusion: Chrysophanol liposomes have a significant protective effect on hippocampal neurons after cerebral ischemia and reperfusion injury. The mechanism may be related to increasing the expression of Bcl-2, reducing caspase-3 and Bax. Reference|Related Articles|Metrics

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A Review on the Neuroprotective Effects of Curcumin ZHAO Li-yan1，YU Xiu-juan1，HAN Tian-yun2，ZHANG Wan-ming1 Acta Neuropharmacologica 2012, 2 (2): 58-64. Abstract（ 6240） PDF（1077KB）（ 2532） Curcumin is a low molecular weight polyphenol compound derived from the rhizome of the plant Curcuma longa. Curcumin was reported to have anti-inflammatory，anti-oxidation and other pharmacological effects.In recent years, curcumin has also been shown to be effective in several neurological disorders, such as Alzheimer's disease, Parkinson's disease, neuropathic pain, and neuroblastoma. This paper reviewed the neuroprotective effects and the potential therapeutic mechanisms of curcumin. Reference|Related Articles|Metrics

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Behavioral Pharmacology: History and Current Status LI Jun-xu Acta Neuropharmacologica 2011, 1 (1): 55-64. Abstract（ 6164） PDF（1258KB）（ 4148） As a branch of pharmacology，behavioral pharmacology has been stepping into its 50s. Since the publication of the hallmark paper of this field in 1955，behavioral pharmacology has seen a steady，vibrant and healthy development. This review traced back into 1950s，summarizing the major events during the history of behavioral pharmacology，and discuss the current status in this field. The paper also discussed several issues related to behavioral pharmacology research. Reference|Related Articles|Metrics

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Neuron-synapse loss and dementias ZHANG Juntian Acta Neuropharmacologica 2011, 1 (1): 1-15. Abstract（ 5925） PDF（35118KB）（ 2146） Basic and clinical study of Alzheimer’s disease showed that senile plagues and neurofibrillary tangle are not related to the degree of cognitive impairment. Synaptic loss occur in Alzheimer’s disease and other neurodegenerative dementias which block LTP，induce neuropsychological dysfunction and memory deficit . Neuron-synapses or synaptic loss was considered as main cause of dementias. Several hidden toxins such as oligomer of Aβ and phosphorylated Tau,glutamate receptor at extrasynaptic region and shank protein can lead to synaptic loss. Therefore，strategy for AD treatment is that ① To clean oligomer by native oligomer of Aβ immunotherapy. ②To maintain the normal homeostasis of synaptic protein by mTOR(a protein kinase) and UPS. ③To activate synaptic NMDA receptors or block extrasynaptic NMDA receptors. ④To increase hippocampal neurogenesis and synaptogenesis. In our recent study，ginsenoside Rg1 and Ppt were proved to increase synaptic plasticity in both efficacy and structure as well as increase neurogenesis both in vitroand in vivo ，under physiological and pathological circumstances，indicating that they are promising agents for preventing and treatment of dementias and many kinds of memory impairment. Reference|Related Articles|Metrics

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Effects of nicotine analog ZY-1 on β-amyloid production and learning and memory in transgenic Alzheimer disease mice NIE Hui-Zhen, WANG Ze-Jian, ZHAO Wen-Juan, LU Jin-Miao, ZHANG Can, LUO Qing-He, WANG Yu-Liang, GAO Xiang, YIN Ming Acta Neuropharmacologica 2011, 1 (1): 26-31. Abstract（ 5730） PDF（1522KB）（ 3398） Objective:To observe the effects of ZY-1, a nicotine analogue, on in vitro receptor binding and β-amyloid (Aβ) production and in vivo transgenic Alzheimer’s disease mice. Methods:Receptor binding assay was carried out in SH-EP1-α4β2 nAChR cell line highly expressing α4β2 nAChR; Western blotting was used to detect the effects of ZY-1 on amyloid protein production in the SH-EP1-α4β2 nAChR cell line transfected with APP695 plasmid; and effects of ZY-1 on learning and memory were measured in B6C3-Tg（APPswe, PSEN1dE9）85Dbo/J mice. Results:1. Receptor binding assay showed that Ki is 21.5 n mol•L-1, suggesting specific binding of ZY-1 to α4β2 nAChR; 2. ZY-1(1 μmol•L-1) reduced intracellular production of Aβ; 3. Middle (0.50 mg•kg-1) and high dose (0.75 mg•kg-1) of ZY-1 improved learning and memory of transgenic mice in Morris water maze and platform test. Conclusion:ZY-1 might be of potential to be an AD therapeutic agent, but the druggability remains to be further confirmed. Reference|Related Articles|Metrics

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Cultivation and identification of neural stem cells cultivated by the methods of neurospheres and adherent monolayer cells HAO Jun-Rong, ZHANG Li, QIN Zheng-Hong Journal of Materials Sciences & Technology 2011, 1 (1): 51-55. Abstract（ 5659） PDF（9034KB）（ 3529） Objective:AIM To explore two methods of culturing mouse embryo neural stem cells in vitro and identification of their differentiation． Methods:The neural stem cells were derived from the cortex tissue of mouse embryo at gestation day of 14～16 with two methods: culturing of neurosphere in floating and culturing of monolayer adherent cells. To observe the development of the neural stem cell，the expression of the stem cell marker Nestin and the neural marker MAP-2 and the glial marker GFAP was examined with immunofluorescence. Results:The cultured neural stem cells proliferated．The maintenance of stem cell property was preserved with both methods as revealed by Nestin immunofluorescence. These stem cells are able to differentiate into glial (GFAP positive) and neuronal lineage (MAP-2positive). Conclusion:With the help of growth factors and serum-free technique，the mouse neural stem cells cultivated by methods of neural stem cell spheres and adherent monolayer cells，have potential of proliferation and differentiation. Reference|Related Articles|Metrics

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Animal Models of Alzheimer’s Disease and Pharmacotherapeutics JIN Miao, AN Hong-mei Acta Neuropharmacologica 2011, 1 (6): 28-36. Abstract（ 5515） PDF（1296KB）（ 3473） This paper reviewed recent progress in animal models of Alzheimer's disease (AD) and pharmacotherapy of AD. Herein, we summarized the different types of AD animal models based on the pathogenesis of AD, and concluded that there is a lack of full demonstration of the etiology and pathological changes of AD disease in animal models. We also summarized the current available medication treatments of AD. Aβ and Tau protein are still the research focus in the field of AD treatment. Chinese medicine also plays a certain role in the treatment of AD, and shows a good prospect. Reference|Related Articles|Metrics

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Antiproliferation Effects of Petasin on Human Neuroblastoma SK-N-SH Cells Cheng Yue-fang, Wang Cai-fang, Li Wen-jie, Lin Qing, Zhang Qi Acta Neuropharmacologica 2011, 1 (3): 1-6. Abstract（ 5501） PDF（4169KB）（ 2845） Objective:To study the antiproliferation effects of petasin on human neuroblastoma SK-N-SH cells and the possible mechanisms involved. Methods:The inhibitory effects of petasin on proliferation of tumor cells was detected by SRB assay; the effects ofpetasin on cell cycle arrest of SK-N-SH were measured by flow cytometry; the effects of apoptosis were examined by Hochest 33258 staining and flow cytometry and the phosphorylationof ERK1/2 of SK-N-SH was determined bywestern blotting. Results:Compared to that of other cancer cell lines such as SGC7901, SPC-A-1, SMMC 7721, Ec9706, SK-N-BE (2) and U251, the proliferation of SK-N-SH cells were strongly inhibited by petasin. After treated with petasin, the cell cycle of SK-N-SH arrested in G0/G1 phase, and there was no apoptosis detected either by Hoechst 33258 staining or by flow cytometry analysis. Finally, the phosphorylation of ERK1/2 was decreased by pretreatment with petasin in a dose-dependent way. Conclusion:Petasin is a potential anti-tumor of natural compounds, and shows the strong antiproliferation effect on SK-N-SH cells without inducing apoptosis. The inhibition of ERK1/2 phosphorylation might be involved in the antiproliferation effects of petasin. Reference|Related Articles|Metrics

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The Effects of Tenuigenin on Expression of nAChRα4 and PSD95 in Alzheimer’s Disease Model Rats Li Xiao-feng, Zhao Da-peng, Chen Shu-sha, Jing Wei, Li Xin-yi ACTA NEUROPHARMACOLOGICA 2011, 1 (3): 16-22. Abstract（ 5452） PDF（9007KB）（ 2742） Objective：To investigate the effects and the underlying mechanisms of Tenuigenin on Alzheimer’s disease by observing the effects of Tenuigenin(TEN) on expression of nicotinic acetylcholine receptor subunit alpha-4 (nAChRα4) and postsynaptic density 95(PSD-95) in Alzheimer’s disease model rat. Methods：32 male Wistar rats were divided randomly into four groups: control group，model group，12.5 mg·mL -1dose TEN group and 37.5 mg·mL -1dose TEN group. The rat model with Alzheimer’s disease was made by injecting ibotenic acid into Meynert basal nuclei of aging rat induced by D-gal.The expressions of nAChRα4 and PSD-95 in the hippocampus CA1 were measured by immunohistochemistry method. Results：Compared with the control group，the average gray-scale values of hippocampus CA1 nAChRα4 and PSD-95 in the model group were increased significantly and the average optical density was decreased obviously ( P<0.01). Compared with the model group，the average gray-scale values in the hippocampus CA1 of 37.5 mg·mL -1dose TEN group and 12.5 mg·mL -1dose TEN group were obviously decreased and the average optical density was increased significantly ( P<0.05). Meanwhile，the average gray-scale value within the hippocampus CA1 of 37.5 mg·mL -1dose TEN group was significantly less than that in 12.5 mg·mL -1dose TEN group，but more distinct than that on the average optical density aspect ( P<0.01). Conclusion：TEN can dose-dependently increase the expression of CA1 area nAChRα4 and PSD-95 in Alzheimer’s disease model rats，which may partly explain the beneficial effects of TEN on cognitive function. Reference|Related Articles|Metrics

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Methods and Evaluation of Animal Models of Cerebral Ischemia and Cerebral Ischemia Reperfusion Injury Wang Shu, Zhang Li Acta Neuropharmacologica 2011, 1 (3): 31-40. Abstract（ 5160） PDF（1126KB）（ 5926） Cerebrovascular disease is a clinically common disease and frequently-occurring disease. The selection and application of reliable animal models are particularly important in studies for the prevention and treatment of cerebrovascular disease. The types, operation procedures of models, and characteristics of the global cerebral and focal cerebral ischemia and cerebral ischemia reperfusion injury in different animal models were discussed in detail in this paper. The improved Himori method (the model of cerebral ischemia reperfusion was produced in mice by temporarily obstructing bilateral common carotid arteries) and some key steps were especially presented in detail. The evaluation of the application characteristics of existing animal models will help to select the appropriate models of cerebral ischemia and cerebral ischemia reperfusion for studying cerebrovascular disease. Reference|Related Articles|Metrics

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Neuroprotective role of the Alpha 2-Adrenergic Agonist Dexmedetomidine in Ischemic Cerebrovascular Disease HU Min, HE Zhi ACTA NEUROPHARMACOLOGICA 2011, 1 (5): 49-55. Abstract（ 5148） PDF（714KB）（ 3442） Ischemic cerebrovascular disease is a common and frequently encountered disease with high disability and mortality rates, and has severe effects on human’s health and quality of life. Cerebral hypoxic ischemia leads to an increase in the number of damaged or dead neurons. Recent studies have provided considerable evidence that alpha 2-adrenergic agonists can protect the brain neuron from cerebral ischemia/reperfusion injury. However, the exact mechanisms of this protection remain unknown. Activation of the alpha 2-adrenergic receptor may be involved. Dexmedetomidine is a highly selective agonist of the alpha 2-adrenergic receptors with neuroprotective effects. This article reviews the pathophysiological process of ischemic cerebrovascular disease, the molecular pharmacology and the neuroprotective mechanisms of dexmedetomidine. Reference|Related Articles|Metrics

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In VivoApplication of Two-photon Microscopy in Neuropharmacological Research ZHAO Jun,WANG Jin-hui Acta Neuropharmacologica 2012, 2 (1): 45-64. Abstract（ 5094） PDF（6504KB）（ 5892） Two-photon microscope is an useful and advanced tool for noninvasive deep fluorescence imaging in the intact brain tissue of living animals. Due to nonlinear two-photon effects, two-photon microscope enables long-term imaging in vivowith deeper detection, higher signal-to-noise ratio and lower photodamage, compared to wide-field and confocal microscopy. Two-photon microscopy can provide high-resolution images to study cellular and subcellular structure and function, including morphology, mobility and intracellular ions of cells. On the other hand, large scale two-photon imaging of cell population reveals the network construction and activity dynamics with single-cell resolution, which makes two-photon microscopy a high throughput tool in system pharmacology. Moreover, two-photon microscopy can offer some precise optical operations, such as photolysis, photoactivation, phototransfection and photodamage. Here, we give an introduction to the principles of two-photon microscopy and its in vivoapplications in neuroscience and neuropharmacology researches. Reference|Related Articles|Metrics

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Rosiglitazone Improves Cognitive Impairment in Streptozotocin-induced Diabetic Mice and its Mechanisms ZHANG Ting-ting，LIU Li-ping，JIANG Li-ying，HU Wei，LONG Yan，HONG Hao Acta Neuropharmacologica 2011, 1 (2): 1-6. Abstract（ 5049） PDF（1263KB）（ 3061） Objective: To investigate the effects of rosiglitazone on cognitive function in streptozotocin-induced diabetic mice and the underlying mechanisms. Methods: Diabetic mice induced by a single intravenous injection of streptozotocin（150 mg• kg -1body weigh）were used as animal model of type 1 diabetes. Diabetic mice with hyperglycemia（>11.1 mmol•L -1）were randomly divided into three groups,including untreated diabetes group, rosiglitazone( 3.2 mg•kg -1and 1.6 mg•kg -1)treated groups（10~12 mice/group）. After orally administration of rosiglitazone for 6 w, rosiglitazone-treated diabetic mice, untreated diabetic mice and non-diabetic controls were tested in the Morris water maze and Y maze. The serum insulin，the levels of Aβ 40，Aβ 42and BACE1 in hippocampus and cortex were determined by ELISA assays，and the blood glucose was measured by the glucose oxidase method. Results: Both water maze and Y maze learning were impaired in diabetic mice. In Morris water maze, rosiglitazone（3.2 mg• kg -1）significantly decreased the escape latency（ P<0.05）and increased the time spent in the platform quadran（ P<0.05）compared with the vehicle diabetic group. Rosiglitazone（3.2 mg• kg -1）also significantly increased the number of correct（ P<0.05）in Y maze test. Rosiglitazone treatment did not decrease the blood glucose and serum insulin of diabetic mice. Rosiglitazone（3.2 mg• kg -1）significantly decreased the Aβ 40（ P<0.05, P<0.05）and Aβ 42（ P<0.05, P<0.05）levels in both hippocampus and cerebral cortex of diabetic mice, without reducing the increased BACE1 level. Conclusion: Rosiglitazone at the dosage of 3.2 mg• kg -1improves cognitive impairments in streptozotocin-induced diabetic mice via the alleviation of the Aβ burden in the brain. Reference|Related Articles|Metrics

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Involvement of Kir6.2-composing ATP-sensitive potassium channels in phencyclidine-induced negative symptoms of schizophrenia DAI Ting, CHEN Zhong-Guo, DUAN Lei, DING Jian-Hua, FAN Yi, HU Gang ACTA NEUROPHARMACOLOGICA 2011, 1 (1): 31-38. Abstract（ 5005） PDF（1811KB）（ 3848） Objective :ATP-sensitive potassium (K-ATP) channels are crucial for dopaminergic and glutamatergic transmission，which has been demonstrated to be the important feature of pathophysiology in schizophrenia. We studied the effects of K-ATP channels on the phencyclidine (PCP)-induced changes in the forced swimming test (FST，an animal model of negative symptoms of schizophrenia)，using mice with knockout of the Kir6.2 (a pore-forming subunit of neuronal K-ATP channel). Methods:After repeated PCP (10 mg·kg -1， i.p.daily for 14 days) administration，The FST were used to assess depression-related behaviors associated with negative symptoms. Striatal dopamine and dopamine turnover were measured by high pressure liquid chromatography with electrochemical detection. Cell proliferation in the subgranular zone (SGZ) was determined by bromodeoxyuridine immunohistochemistry. The expressions of total Akt and phosphorylation Akt were evaluated using Western blot. Results:After repeated PCP administration，the enhancement of immobility induced by the FST was attenuated in Kir6.2 knockout mice. Meanwhile，Kir6.2 knockout decreased striatal dopamine turnover，whereas wild-type mice exhibited an augmentation in response to PCP treatment. Furthermore，Kir6.2 knockout could prevent the inhibition of neural stem cell proliferation in the SGZ and suppressed the PCP-induced phosphorylation of Akt Ser473. Conclusion:These results suggest a possible implication of Kir6.2-composing K-ATP channels dysfunction in the pathogenesis of negative symptoms associated with schizophrenia. Reference|Related Articles|Metrics

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Application of Uniform Design-High Throughput Screening in Research of Neuroprotective Effects of Five Ginsenoside and Notoginsenoside Components Song Zhi-bin, Zhang Dan-shen ACTA NEUROPHARMACOLOGICA 2011, 1 (3): 7-15. Abstract（ 4999） PDF（2258KB）（ 3089） Objective：To evaluate the application of uniform design-high throughput screening technology for screening the active ingredients of traditional Chinese medicine. Methods：Weperformed uniform design compatibility study on four different saponin monomers ginsenoside Re, Rb1, Rg1, Rg3 and one notoginsenoside R1 each atsix concentrations (1×10 -4~1×10 -9mol·L -1), and their neuroprotective effects were assessed on the damaged nerve cells deprived of the serum. The obtained optimal combination of the ingredients from the above cell study was subjected to further animal tests for their pharmacological effects against the damages induced by cerebral ischemia reperfusion of mice model; the passive avoidance test, the hypoxia tolerance test were performed and the levels of aging-related enzymes in serum, brain and heart tissue were determined for assessing the effects of these ingredients. Results： The best combination samples (A11, A12, P5) obtained from cell screening experiment, have higher potency (cell survival ratio﹥90%) than any of five individual saponin monomers and vitamin E (the highest cell survival ratio was 78%) tested at a high concentration of 1×10 -4mol·L -1; these combinations significantly improved the learning and memory impairment induced by cerebral ischemia reperfusion injury, enhanced the hypoxia tolerance ability, increased the activity of superoxide dismutase, reduced the content of nitric oxide and maintained stability stable level of glutamic-pyruvic transaminase and lactic dehydrogenase ( P<0.01~0.05). Conclusion： Uniform design compatibility and the traditional Chinese medicine compoundcompatibility have similarities. The best three combination samples obtained from five saponins by high-throughput screening show protective effect on cerebral ischemia reperfusion injury. Uniform design-high throughput screening technology is a reliable technology for massive potency screening of active ingredients of traditional Chinese medicine and compounds. Reference|Related Articles|Metrics

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Antiemetic Effect and Mechanism of Small Pinelliae Decoction on Mink Vomit Model Ren Xu-ying，Mou Qun-fang，Luo Yi-ren，Wang Jue，Wang Yue，Zhang Fang Acta Neuropharmacologica 2011, 1 (3): 23-26. Abstract（ 4984） PDF（1160KB）（ 3108） Objective： To study the antiemetic effect of Small Pinelliae Decoction (SPD) and its mechanism. Methods： he active ingredients were extracted from TSPD(pinellia tuber:ginger=1:1) to make the granules. Cisplatin(7.5 mg·kg -1, ip) and apomorphine(1.6 mg·kg -1, ip) were used to prepare mink vomiting model. After 30 min of SPD (equivalent to 4.0, 1.0 g·kg -1crude drug) ig. adminstration, minks were administered of cisplatin or morphine to study the inhibitory effect and mechanism of SPD on the two models of vomiting. Results： SPD could inhibit acute and delayed vomiting induced by cisplatin (within 72 h) in the minks, reduce the number of retching and vomiting( P<0.01), prolong the latency to vomit ( P<0.01), and inhibit the expression of NK 1receptor in central (the area postrema) and peripheral (ileum tissue) tissues ( P<0.05). SPD could also inhibit vomiting induced by apomorphine (within 6 h) ( P<0.01), reduce significantly the ratio of vomiting ( P<0.05) and did not affect the latency to vomit. Conclusion： SPD can inhibit vomiting induced by cisplatin and apomorphine, and its mechanism is related to the inhibition of central and peripheral NK 1receptor expression. Reference|Related Articles|Metrics

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Mitochondria and Neurodegenerative Diseases Zhou Xiao-wen, Su Chao-fen, Luo Huan-min ACTA NEUROPHARMACOLOGICA 2011, 1 (3): 41-46. Abstract（ 4947） PDF（1083KB）（ 4099） The neurodegenerative diseases are usually caused by the loss of the neurons and/or their myelin sheath, but the pathogenesis of these diseases are still indeterminate. Studies so far has proved that mitochondrial dysfunction and energy metabolism disorders are early pathological phenomena. This review concentrates on two of the most prevalent neurodegenerative diseases: Alzheimer’s disease (AD) and Parkinson’s disease(PD) and would be aimed to discuss the role of mitochondrial in pathogenesis of neurodegenerative diseases, providing new direction for further research. Reference|Related Articles|Metrics

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Glucocorticoids and Hippocampal Structural Plasticity CHEN Lin，DU Li-jun，ZHAO Yu-nan Acta Neuropharmacologica 2011, 1 (2): 58-64. Abstract（ 4938） PDF（1023KB）（ 3368） Chronic high dose glucocorticoid exposure produces the major disruption to the hippocampal structural plasticity（such as plastic changes in spine and dendrite morphology, astrocyte as well as adult neurogenesis）, which can be reversed by anti-glucocorticoid therapy,indicating that glucocorticoids play a crucial role in chronic stress-induced impairment of hippocampal structural plasticity. Thus, one way to avoid the variable effects of stress exposure on animal behavior is developed by using exogenous corticosterone administration as a means to enhance efficiency and stability of animal model. Interestingly, short-term or acute glucocorticoid exposure has the ability to enhance structural plasticity, suggesting that the regulation of glucocorticoids on hippocampal structural plasticity is bidirectional. Reference|Related Articles|Metrics