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Aqueous Extract of Saffron (<i>Crocus sativus</i>) Increases Brain Dopamine and glutamate Concentrations in Rats

Journal of Behavioral and Brain Science 2013年第3期3卷 315-319页

作者： Hosseinali Ettehadi Seyedeh Nargesolsadat Mojabi Mina Ranjbaran Jamal Shams Hedayat Sahraei Mahdi Hedayati Farzad Asefi Department of Physiology Faculty of Medicine Shahid Beheshti University of Medical Sciences Tehran Iran Department of Psychiatry Faculty of Medicine and Neuroscience Research Center Shahid Beheshti University of Medical Sciences Tehran Iran Fat Research Center Shahid Beheshti University of Medical Sciences Tehran Iran Institute of Science and Technology Tehran Iran Neuroscience Research Center Baqyiatallah (a.s.) University of Medical Sciences Tehran Iran

Recent studies involving human and animal models have identified that saffron helps in the improvement of depression. Antidepressants are known to function in part by increasing brain serotonin, norepinephrine and dopamine concentrations. Therefore, to identify the cellular and molecular mechanism(s) underlying this property of saffron, we measured changes in rat brain dopamine, serotonin, norepinephrine and glutamate concentrations after administration of varying doses of an aqueous extract of saffron stigma. Male Wistar rats (250 ± 30 g) were administered a single dose of saffron extract (5, 25, 50, 100, 150, and 250 mg/kg, i.p.), fluoxetine (10 mg/kg, i.p.), and/or desipramine (50 mg/kg, i.p.) and were sacrificed 30 min later. Brains were removed, homogenized, and centrifuged at 4?C. The supernatant was used for subsequent neurotransmitter detection by ELISA. Our results indicated that the aqueous extract of saffron (50, 100, 150 and 250 mg/kg, i.p.) increased brain dopamine concentration in a dose-dependent manner compared with saline. In addition, the brain glutamate concentration increased in response to the highest dose of the extract (250 mg/kg, i.p.). Interestingly, the extract had no effect on brain serotonin or norepinephrine concentration. Our findings show that the aqueous extract of saffron contains an active component that can trigger production of important neurotransmitters in brain, namely, dopamine and glutamate. In addition, these results provide a cellular basis for reports concerning the antidepressant properties of saffron extract in humans and animals.

关键词： Saffron glutamate Dopamine Norepinepherine Serotonin

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Relationship between glutamate in limbic system and hypothalamuspituitary-adrenal axis after middle cerebral artery occlusion in rats

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Journal of Medical Colleges of PLA(China) 1998年第3期13卷 171-174页

作者：何明利陈曼娥王景周

Objective To study the features of the activity changes of glutamate (GLu ) in the hippocampusand hypothalamus and its effects on the activation of the hypothalamus-pituitary-adrenal axis (HPA ) duringacute cerebral ischemia (ACI ). Methods: The changes of Glu content, corticotrophin releasing hormone(CRH ) mRNA expression level and adrenocorticotropic hormone (ACTH ) concentration were determinedwith high-performance liquid chromatography (HPLC ) and in situ hybridization in different time intervals after middle cerebral artery occlusion (MCAO) in rats. Results: Glu content was increased rapidly in the hippocampus and hypothalamus 15 min after MCAO and reached the peak (the average Glu content in the hippocarnpus and hypothalamus were 21. 50± 2. 88 mg/g wt and 14. 20±2. 58 mg/g wt respectively) in the lsthour after MCAO and it returned rapidly to the base line level after reperfusion. The Gln content in the hippocampus and hypothalamus went up once more in the 24th hour of reperfusion, remained at a relatively highlevel till the 48th hour of reperfusion and then declined gradually. The expression level of CRH mRNA wasmarkedly enhanced in the temporal cortex, hippocampus and hypothalamus in the lst hour after MCAO andthis condition was kept on till the 96th hour of reperfusion. In the same time, the plasma level of ACTH wasrelatively increased. In the peak stage of reperfusion injury,there was a positive correlation of the Glu contentin the hypothalamus with the number of positive cells of CRH mRNA expression and the plasma level of ACTH. Conclusion: The central CRH system is possible to locate mainly in the limbic system and Gln might beone of the factors to induce excessive excitable stress response of the HPA axis.

关键词： cerebral ischemia glutamate hypothalamus--pituitary--adrenal axis

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CHEMOSENSITIVITY OF THE FROG ISTHMIC NEURONS TO ACETYLCHOLINE,glutamate AND GLYCINE

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Chinese Science Bulletin 1985年第12期30卷 1681-1683页

作者：王书荣颜坤许红艳 Institute of Biophysics Academia Sinica Beijing

Several studies have shown that acetylcholine (ACh) is an excitatory transmitter in the anuran optic tectum; the nucleus isthmus (NI) is an important source of tectal cholinergic activity; an d acetylcholinesterase (A... 详细信息

关键词： AChE acetylcholine cholinergic transmitter nucleus excitatory optic inhibiting glutamate neuronal

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NMDA and AMPA receptors mediate intracellular calcium increase in rat cortical astrocytes

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Acta Pharmacologica Sinica 2004年第6期25卷 12-18页

作者： Bo HU, Sheng-gang SUN2, E-tang TONGNeurology Department, Union Hospital, Tongji College, Huazhong University of Science and Technology, Wuhan 430022, China Neurology Department Union Hospital Tongji College Huazhong University of Science and Technology Wuhan 430022

AIM: To study the effect of glutamate on the intracellular calcium signal of pure cultured rat astrocytes and the roleof N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) re-ceptors in the procedure. METHODS: The fluorescence of calcium was measured by Fura-2/AM (F345/F380).RESULTS: L-glutamate induced [Ca2+]i increase in most of the cells in concentration- and time-dependent manner.NMDA 50 mmol/L induced the fluorescence increase by almost three to four times, while the effect of AMPA 50mmol/L was just half of that of D-(-)-2-amino-5-phosphonopentanoic acid (D-AP-5; a selective antagonist of theNMDA receptor). 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX, a selective antagonist of the AMPA receptor)abolished the effects of NMDA and AMPA, respectively. D-AP-5 and CNQX simultaneously or respectively attenu-ated the effect of L-glutamate at different degrees, but could not abolish it entirely. CONCLUSION: glutamatemodulated intracellular Ca2+ of pure cultured rat astrocytes through different pathways. The activation of NMDAand AMPA receptors took part in the complex mechanisms.

关键词： glutamate astrocytes NMDA receptors AMPA receptors calcium

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Ferrostatin-1 protects HT-22 cells from oxidative toxicity

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Neural Regeneration Research 2020年第3期15卷 528-536页

作者： Jun Chu Chen-Xu Liu Rui Song Qing-Lin Li Xin’an Key Laboratory of Medicine Ministry of Education Anhui University of Chinese Medicine

Ferroptosis is a type of programmed cell death dependent on iron.It is different from other forms of cell death such as apoptosis,classic necrosis and autophagy.Ferroptosis is involved in many neurodegenerative diseases.The role of ferroptosis in glutamate-induced neuronal toxicity is not fully understood.To test its toxicity,glutamate(1.25–20 mM)was applied to HT-22 cells for 12 to 48 hours.The optimal experimental conditions occurred at 12 hours after incubation with 5 mM glutamate.Cells were cultured with 3–12μM ferrostatin-1,an inhibitor of ferroptosis,for 12 hours before exposure to glutamate.The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Autophagy was determined by monodansylcadaverine staining and apoptosis by caspase 3 activity.Damage to cell structures was observed under light and by transmission electron microscopy.The release of lactate dehydrogenase was detected by the commercial kit.Reactive oxygen species were measured by flow cytometry.Glutathione peroxidase activity,superoxide dismutase activity and malondialdehyde level were detected by the appropriate commercial kit.Prostaglandin peroxidase synthase 2 and glutathione peroxidase 4 gene expression was detected by real-time quantitative polymerase chain reaction.Glutathione peroxidase 4 and nuclear factor erythroid-derived-like 2 protein expression was detected by western blot analysis.Results showed that ferrostatin-1 can significantly counter the effects of glutamate on HT-22 cells,improving the survival rate,reducing the release of lactate dehydrogenase and reducing the damage to mitochondrial ultrastructure.However,it did not affect the caspase-3 expression and monodansylcadaverine-positive staining in glutamate-injured HT-22 cells.Ferrostatin-1 reduced the levels of reactive oxygen species and malondialdehyde and enhanced superoxide dismutase activity.It decreased gene expression of prostaglandin peroxidase synthase 2 and increased gene expression of glutathione peroxidase 4 and protein ex

关键词： ferroptosis ferrostatin-1 glutamate glutathione peroxidase 4 HT-22 cell oxidative toxicity prostaglandin peroxidase synthase 2 reactive oxygen species

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Regional Metabolic Patterns of Abnormal Postoperative Behavioral Performance in Aged Mice Assessed by XH-NMR Dynamic Mapping Method

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Neuroscience Bulletin 2020年第5期36卷 25-38页

作者： Taotao Liu Zhengqian Li Jindan He Ning Yang Dengyang Han Yue Li Xuebi Tian Huili Liu Anne Manyande Hongbing Xiang Fuqiang Xu Jie Wang Xiangyang Guo Department of Anesthesiology Peking University Third HospitalBeijing 100191China Key Laboratory of Magnetic Resonance in Biological Systems State Key Laboratory of Magnetic Resonance and Atomic and Molecular PhysicsWuhan Institute of Physics and MathematicsChinese Academy of SciencesWuhan 430071China Department of Anesthesiology and Pain Medicine Tongji HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030China School of Human and Social Sciences University of West LondonMiddlesex TW89GAUK University of Chinese Academy of Sciences Beijing 100049China The Second Hospital of Shijiazhuang Shijiazhuang 050051China

Abnormal postoperative neurobehavioral performance(APNP)is a common phenomenon in the early postoperative period.The disturbed homeostatic status of metabolites in the brain after anesthesia and surgery might make a significant contribution to APNP.The dynamic changes of metabolites in different brain regions after anesthesia and surgery,as well as their potential association with APNP are still not well understood.Here,we used a battery of behavioral tests to assess the effects of laparotomy under isoflurane anesthesia in aged mice,and investigated the metabolites in 12 different sub-regions of the brain at different time points using proton nuclear magnetic resonance('H-NMR)spectroscopy.The abnormal neurobehavioral performance occurred at 6 h and/or 9 h,and recovered at 24 h after anesthesia/surgery.Compared with the control group,the altered metabolite of the model group at 6 h was aspartate(Asp),and the difference was mainly displayed in the cortex;while significant changes at 9 h occurred predominantly in the cortex and hippocampus,and the corresponding metabolites were Asp and glutamate(Glu).All changes returned to baseline at 24 h.The altered metabolic changes could have occurred as a result of the acute APNP,and the metabolites Asp and Glu in the cortex and hippocampus could provide preliminary evidence for understanding the APNP process.

关键词： Abnormal postoperative neurobehavioral performance 1H-NMR Metabolite Aspartate glutamate

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Neuroprotective effects of Asiaticoside

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Neural Regeneration Research 2014年第13期9卷 1275-1282页

作者： Feng-yan Qi Le Yang Zhen Tian Ming-gao Zhao Shui-bing Liu Jia-ze An Department of Pharmacology School of Pharmacy Fourth Military Medical University of Chinese PLA Department of Hepatobiliary Surgery Xijing Hospital Fourth Military Medical University of Chinese PLA

In the central nervous system, Asiaticoside has been shown to attenuate in vitro neuronal damage caused by exposure to β-amyloid. In vivo studies demonstrated that Asiaticoside could attenuate neurobehavioral, neurochemical and histological changes in transient focal middle cerebral artery occlusion animals. In addition, Asiaticoside showed anxiolytic effects in acute and chronic stress animals. However, its potential neuroprotective properties in glutamate-induced excitotoxicity have not been fully studied. We investigated the neuroprotective effects of Asiaticoside in primary cultured mouse cortical neurons exposed to glutamate-induced excitotoxicity invoked by N-methyl-D-aspartate. Pretreatment with Asiaticoside decreased neuronal cell loss in a concentration-dependent manner and restored changes in expression of apoptotic-related proteins Bcl-2 and Bax. Asiaticoside pretreatment also attenuated the upregulation of NR2B expression, a subunit of N-methyl-D-aspartate receptors, but did not affect expression of NR2A subunits. Additionally, in cultured neurons, Asiaticoside significantly inhibited Ca^2＋ influx induced by N-methyl-D-aspartate. These experimental findings provide preliminary evidence that during excitotoxicity induced by Nmethyl-D-aspartate exposure in cultured cortical neurons, the neuroprotective effects of Asiaticoside are mediated through inhibition of calcium influx. Aside from its anti-oxidant activity, down-regulation of NR2B-contalning N-methyl-D-aspartate receptors may be one of the underlying mechanisms in Asiaticoside neuroprotection.

关键词： nerve regeneration brain injury Asiaticoside apoptosis N-methfl-D-aspartate glutamate neurotransmitter neurotoxicity calcium imaging B^t-2 Bax NSFC grant neural regeneration

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Adolescent stress increases depression-like behaviors and alters the excitatory-inhibitory balance in aged mice

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Chinese Medical Journal 2019年第14期132卷 1689-1699页

作者： Hong-Li Wang Ya-Xin Sun Xiao Liu Han Wang Yu-Nu Ma Yun-Ai Su Ji-Tao Li Tian-Mei Si National Clinical Research Center for Mental Disorders(Peking University Sixth Hospital/Institute of Mental Health)and the Key Laboratory of Mental Health Ministry of Health(Peking University)Beijing 100191China The Sixth People's Hospital of Hebei Province BaodingHebei 071000China

Background:Depression affects approximately 5% of elderly people and its etiology might be related to chronic stress exposure during neurodevelopmental periods.In this study,we examined the effects of adolescent chronic social stress in aged mice on depressive behaviors and the excitatory-inhibitory (E/I) balance in stress-sensitive regions of the brain.Methods:Sixty-four adolescent,male C57BL/6 mice were randomly assigned to either the 7-week (from post-natal days 29 to 77) social instability stress (stress group,n =32) or normal housing conditions (control group,n =32).At 15 months of age,16 mice were randomly selected from each group for a series of behavioral tests,including two depression-related tasks (the sucrose preference test and the tail suspension test).Three days following the last behavioral test,eight mice were randomly selected from each group for immunohistochemical analyses to measure the cell density of parvalbumin (PV+)-and calretinin (CR+)-positive gamma-aminobutyric-acid (GABA)ergic inhibitory inter-neurons,and the expression levels of vesicular transporters of glutamate-1 (VGIuT1) and vesicular GABA transporter (VGAT) in three stress-sensitive regions of the brain (the medial pre-frontal cortex [mPFC],hippocampus,and amygdala).Results:Behaviorally,compared with the control group,adolescent chronic stress increased depression-like behaviors as shown in decreased sucrose preference (54.96 ± 1.97% vs.43.11 ± 2.85%,t(22)=3.417,P =0.003) and reduced latency to immobility in the tail suspension test (92.77 ± 25.08 s vs.33.14 ± 5.95 s,t(25)=2.394,P =0.025),but did not affect anxiety-like behaviors and pre-pulse inhibition.At the neurobiologic level,adolescent stress down-regulated PV+,not CR+,inter-neuron density in the mPFC (F(1,39)=19.30,P 10.09,all P < 0.004),which suggests stress-induced hy

关键词： Adolescence Aging Depression Inter-neuron Stress Vesicular glutamate transporter-1

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ATP11B deficiency leads to impairment of hippocampal synaptic plasticity

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Journal of Molecular Cell Biology 2019年第8期11卷 688-702页

作者： Jiao Wang Weihao Li Fangfang Zhou Ruili Feng Fushuai Wang Shibo Zhang Jie Li Qian Li Yajiang Wang Jiang Xie Tieqiao Wen Laboratory of Molecular Neural Biology School of Life Sciences Shanghai University Shanghai 200444 China School of Computer Engineering and Science Shanghai University Shanghai 200444 China

Synaptic plasticity is known to regulate and support signal transduction between neurons, while synaptic dysfunction contributes to multiple neurological and other brain disorders;however, the specific mechanism underlying this process remains unclear. In the present study, abnormal neural and dendritic morphology was observed in the hippocampus following knockout of Atpllb both in vitro and in vivo. Moreover, ATP11B modified synaptic ultrastructure and promoted spine remodeling via the asymmetrical distribution of phosphatidylserine and enhancement of glutamate release, glutamate receptor expression, and intracellular Ca^2+ concentration. Fuithermoe experimental results also indicate that ATP11B regulated synaptic plasticity in hippocampal neurons through the MAPK14 signaling pathway. In conclusion, our data shed light on the possible mechanisms underlying the regulation of synaptic plasticity and lay the foundation for the exploration of proteins involved in signal transduction during this process.

关键词： ATP11B synaptic plasticity glutamate receptors MAPK14 signaling pathway

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Thymosin Alpha-1 Inhibits Complete Freund’s Adjuvant-Induced Pain and Production of Microglia-Mediated Pro-inflammatory Cytokines in Spinal Cord

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Neuroscience Bulletin 2019年第4期35卷 637-648页

作者： Yunlong Xu Yanjun Jiang Lin Wang Jiahua Huang Junmao Wen Hang Lv Xiaoli Wu Chaofan Wan Chuanxin Yu Wenjie Zhang Jiaying Zhao Yinqi Zhou Yongjun Chen South China Research Center for Acupuncture and Moxibustion Medical College of Acu-Moxi and Rehabilitation Guangzhou University of Chinese Medicine Guangzhou 510006 China College of Basic Medical Science Guangzhou University of Chinese Medicine Guangzhou 510006 China The First Clinical College of Guangzhou University of Chinese Medicine Guangzhou 510006 China Graduate College Guangzhou University of Chinese Medicine Guangzhou 510006 China

Activation of inflammatory responses regulates the transmission of pain pathways through an integrated network in the peripheral and central nervous systems.The immunopotentiator thymosin alpha-1(Tal)has recently been reported to have anti-inflammatory and neuroprotective functions in rodents.However,how Tα1 affects inflammatory pain remains unclear.In the present study,intraperitoneal injection of Tal attenuated complete Freund's adjuvant(CFA)-induced pain hypersensitivity,and decreased the up-regulation of pro-inflammatory cytokines(TNF-α,IL-1β,and IL-6)in inflamed skin and the spinal cord.We found that CFA-induced peripheral inflammation evoked strong microglial activation,but the effect was reversed by Tα1.Notably,Tα1 reversed the CFA-induced up-regulation of vesicular glutamate transporter(VGLUT)and down-regulated the vesicular γ-aminobutyric acid transporter(VGAT)in the spinal cord.Taken together,these results suggest that Tα1 plays a therapeutic role in inflammatory pain and in the modulation of microgliainduced pro-inflammatory cytokine production in addition to mediation of VGLUT and VGAT expression in the spinal cord.

关键词： Thymosin alpha-1 Cytokine Microglia Vesicular glutamate transporter type 2 Vesicular γ-aminobutyric acid transporter

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