瑞舒伐他汀钙对冠心病合并高脂血症患者血清hs-CRP及颈动脉内膜中层厚度的影响

目的:分析不同剂量瑞舒伐他汀钙治疗冠心病合并高脂血症患者的临床效果以及对患者血清hs-CRP和颈动脉内膜中层厚度(IMT)的影响。方法:选择2013年6月-2015年6月在我院接受治疗的冠心病合并高脂血症患者203例,根据用药剂量不同将其分为小剂量组(70例)、中剂量组(64例)及大剂量组(69例),分别采用口服瑞舒伐他汀钙5 mg/次/日、10 mg/次/日和20 mg/次/日进行治疗。观察并比较三组患者治疗前后血脂(TG,TC,LDL-C,HDL-C)、血清hs-CRP及IMT的变化情况。结果:治疗前,三组患者血清hs-CRP,TG,TC,LDL-C,HDL-C以及IMT值比较,差别均无统计学意义(P0.05);治疗后,三组患者血清hs-CRP,TG,TC,LDL-C,HDL-C以及IMT值均较治疗前降低,差异具有统计学意义(P0.05);大剂量瑞舒伐他汀钙组患者血清hs-CRP,TG,TC,LDL-C,HDL-C以及IMT值显著低于中剂量组和小剂量组,差异具有统计学意义(P0.05);中剂量组患者血清hs-CRP,TG,TC,LDL-C,HDL-C以及IMT值显著低于小剂量组,差异具有统计学意义(P0.05)。结论:瑞舒伐他汀钙能够改善冠心病合并高脂血症患者的血脂水平、降低血清hs-CRP及IMT,并且其疗效与药物剂量存在量效关系。     

阿托伐他汀联合参松养心胶囊治疗老年心力衰竭患者临床疗效及安全性研究

目的:探讨阿托伐他汀联合参松养心胶囊对老年心力衰竭患者的临床疗效及安全性。方法:选取我院心血管内科治疗的老年慢性心力衰竭患者121例,按治疗药物不同分为两组,对照组46例采用西医常规治疗,研究组75例常规治疗基础上给予阿托伐他汀联合参松养心胶囊治疗,记录两组12个月后的临床疗效,治疗后3、6及12个月后的总胆固醇(Total cholesterol,TC)、甘油三酯(Triglyceride,TG)、高密度脂蛋白胆固醇(High density lipoprotein cholesterol,HDL-C)、低密度脂蛋白胆固醇(Low density lipoprotein cholesterol,LDL-C)水平的变化及不良反应的发生情况。结果:与治疗3个月时相比,两组治疗12个月时临床有效率均显著提高,研究组治疗6、12个月后临床有效率均显著高于对照组(85.33%vs. 76.09%, 88%vs. 80.43%,P0.05)。两组治疗后血清TC、TG、LDL-C水平逐步下降,血清HDL-C水平逐步上升,研究组治疗第12月后血清TC、TG及LDL-C水平较对照组显著降低(P0.05),血清HDL-C水平较对照组明显升高(P0.05)。两组在1年观察期内均未见明显肝肾功能损伤及肌溶解,不良反应发生率比较差异无统计学意义(P0.05)。结论:长期使用阿托伐他汀联合参松养心胶囊治疗老年性心力衰竭的临床效果明显优于西医常规治疗,其可有效降低血脂水平,安全性高。     

氨氯地平联合阿托伐他汀钙对高血压合并冠心病的疗效分析

目的:研究氨氯地平联合阿托伐他汀钙对高血压合并冠心病的临床疗效,对该方法的安全性和有效性进行评价。方法:选取80例高血压合并冠心病患者,随机分为两组,即对照组和观察组。对照组患者给予阿托伐他汀钙片,观察组患者给予氨氯地平阿托伐他汀钙片。观察并记录两组患者治疗前后的收缩压、舒张压水平,以及心绞痛发生情况,治疗前后检测患者体内TG、TC、LDL-C及HDL-C表达水平。结果:和对照组患者相比,观察组患者降压作用及心绞痛改善作用均显效率显著提高(P0.05);和治疗前相比,两组患者收缩压、舒张压,以及TG、TC、LDL-C表达水平均显著降低,HDL-C表达水平均显著升高(P0.05);和对照组患者相比,观察组患者治疗后收缩压、舒张压,以及TG、TC、LDL-C表达水平降低更显著,HDL-C表达水平升高更显著(P0.05)。结论:和单独应用阿托伐他汀钙相比,氨氯地平联合阿托伐他汀钙治疗高血压合并冠心病具有更好的的临床疗效,能有效的控制血压及血脂水平。     

大剂量瑞舒伐他汀钙治疗老年冠心病合并高脂血症的疗效观察

目的:研究大剂量瑞舒伐他汀钙治疗老年冠心病合并高脂血症的临床疗效。方法:选取2013年10月到2014年10月我院收治的老年冠心病合并高脂血症患者110例,按照随机数字表法将患者分为研究组和对照组,每组55例。两组患者均给予常规治疗方法进行治疗,对照组增加5 mg瑞舒伐他汀钙进行治疗,研究组增加20 mg瑞舒伐他汀钙进行治疗,均每天1次,晚餐后应用,治疗时间为4个月。比较治疗前后两组血脂水平(胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C))及高密度脂蛋白(HDL-C)及其达标率以及不良反应。结果:治疗后两组TC、TG以及LDL-C均显著降低,HDL-C显著升高,且研究组优于对照组,比较差异具有统计学意义(P0.05);研究组治疗后TC和LDL-C达标率显著高于对照组,两组比较差异具有统计学意义(P0.05);两组不良反应发生率比较差异无统计学意义(P0.05)。结论:大剂量瑞舒伐他汀钙治疗老年冠心病合并高脂血症具有较好的临床疗效,能显著降低患者的血脂水平。     

阿托伐他汀对急性心肌梗塞患者hs-CRP及血脂水平的影响

目的:研究阿托伐他汀对急性心肌梗塞患者超敏C反应蛋白(hs-CRP)及血脂水平的影响。方法:选取2012年1月到2015年1月我院收治的急性心肌梗塞患者80例,按照随机数字表法将患者分为研究组和对照组,每组40例,对照组给予常规治疗,研究组在对照组的基础上给予阿托伐他汀治疗,比较治疗前后两组hs-CRP和总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)和高密度脂蛋白胆固醇(HDL-C)水平。结果:两组治疗后hs-CRP较治疗前显著降低(P0.05),且研究组治疗后hs-CRP显著低于对照组,(P0.05);治疗后两组TC、TG和LDL-C显著低于治疗前,HDL-C显著高于治疗前(P0.05),且治疗后研究组TC、TG和LDL-C显著低于对照组,HDL-C显著高于对照组(P0.05)。结论:阿托伐他汀治疗急性心肌梗塞具有较好的效果,能有效降低hs-CRP水平,改善患者血脂水平。     

瑞舒伐他汀与阿托伐他汀对冠心病高脂血症患者血脂及血浆ADMA水平的影响

目的:探讨瑞舒伐他汀与阿托伐他汀对冠心病高脂血症患者血脂及血浆不对称二甲基精氨酸(ADMA)水平的影响。方法:选取2016年3月-2017年12月四川大学华西医院收治的冠心病高脂血症患者210例为研究对象,随机分为研究组与对照组,每组各105例,研究组患者给予瑞舒伐他汀治疗,对照组给予阿托伐他汀治疗,均连续治疗8周。比较两组患者治疗前及治疗8周后血脂水平、ADMA水平及血清炎症因子水平、血管内皮功能指标水平,记录两组患者的不良反应发生情况。结果:两组患者治疗前及治疗8周后甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)水平比较无统计学差异(P0.05),两组患者治疗8周后TG、TC、LDL-C水平均较治疗前降低(P0.05),而HDL-C水平与治疗前相比无统计学差异(P0.05)。两组患者治疗8周后ADMA、超敏C反应蛋白(hs-CRP)、白介素-6(IL-6)水平均较治疗前降低,且研究组低于对照组(P0.05)。治疗8周后两组患者内皮素-1(ET-1)水平较治疗前降低,一氧化氮(NO)水平较治疗前升高(P0.05),且研究组患者ET-1水平低于对照组,NO水平高于对照组(P0.05)。研究组与对照组患者在治疗期间均未发生难以耐受的不良反应。结论:与阿托伐他汀相比,应用瑞舒伐他汀治疗冠心病高脂血症患者可改善血管内皮功能和TG、TC、LDL-C水平,减轻炎症反应,降低ADMA水平,无严重不良反应发生,值得临床推广。     

中西医结合治疗对T2DM合并CHD患者血糖、血脂及血管内皮功能的影响

目的:探讨中西医结合治疗对2型糖尿病(T2DM)合并冠心病(CHD)患者血糖、血脂及血管内皮功能的影响。方法:将120例T2DM合并CHD患者上随机分为研究组与对照组各60例,在原饮食、运动疗法及降压、降糖治疗方案不变的条件下,对照组加用阿托伐他汀钙片治疗,研究组加用阿托伐他汀钙片与降脂通脉胶囊治疗。检测和比较两组治疗前后总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、空腹血糖(FBG)、餐后2h血糖(2h PBG)、一氧化氮(NO)及内皮素(CE)-1水平的变化。结果:两组治疗后FBG、2h PBG水平均较治疗前明显下降(P0.05),而组间比较差异无统计学意义(P0.05)。两组治疗后TG、TC、LDL-C水平均较治疗前明显下降(P0.05),HDL-C水平均较治疗前明显升高(P0.05),且研究组TG、TC、LDL-C水平显著低于对照组(P0.05),HDL-C水平显著高于对照组(P0.05)。两组治疗后血清NO水平均较治疗前明显升高(P0.05),血清CE水平均较治疗前明显下降(P0.05),且研究组血清NO水平明显高于对照组(P0.05),血清CE水平明显低于对照组(P0.05)。两组治疗过程中均未见明显不良反应。结论:降脂通脉胶囊联合阿托伐他汀可显著改善T2DM合并CHD患者的血脂和血管内皮功能,但不会进一步降低血糖。     

不同剂量阿托伐他汀对冠心病患者心功能、血脂及血清TNF-α、ANF水平的影响

目的:探讨不同剂量阿托伐他汀对冠心病患者心功能、血脂及血清肿瘤坏死因子-α(TNF-α)、心钠素(ANF)水平的影响。方法:选取2016年1月到2017年1月在我院接受治疗的冠心病患者86例,根据随机数字表法将患者分为观察组和对照组,各43例,对照组给予10 mg剂量的阿托伐他汀进行治疗,观察组给予20 mg剂量的阿托伐他汀进行治疗,两组均治疗6个月。比较两组患者治疗前后的左心室舒张末期内径(LVEDD)、左心室射血分数(LVEF)、左心房前后径(LAD)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、TNF-α、ANF水平。对所有患者进行1年的随访,比较患者出现心肌梗死、心律失常、心源性死亡等心血管事件的情况。结果:治疗后两组的LVEDD、LAD、TC、TG、LDL-C、TNF-α、ANF均显著降低,LVEF、HDL-C显著升高(P0.05),治疗后观察组的LVEDD、LAD、TC、TG、LDL-C、TNF-α、ANF低于对照组,LVEF高于对照组(P0.05)。两组的心血管事件发生率比较无统计学差异(P0.05)。结论:两种剂量的阿托伐他汀均能有效的改善冠心病患者的心功能和血脂,降低患者体内的炎症反应,但20 mg剂量的阿托伐他汀效果更佳。     

不同剂量阿托伐他汀对老年急性冠脉综合征患者经PCI术后血清炎症因子水平和内皮功能的影响

目的:探讨不同剂量阿托伐他汀对老年急性冠脉综合征患者经PCI(经皮冠状动脉介入治疗,percutaneous coronary intervention)术后血脂、血清炎症因子水平及血管内皮功能的影响。方法:选取2015年8月至2017年4月我院收治的老年急性冠脉综合征患者80例,依据随机数据表法分为观察组和对照组,每组40例。对照组给予小剂量阿托伐他汀(20 mg/d)治疗,观察组给予大剂量阿托伐他汀(40 mg/d)治疗。比较两组治疗前后总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白胆固醇(low-density lipoprotein,LDL-C)、高密度脂蛋白胆固醇(high-density lipoprotein,HDL-C)、超敏C反应蛋白(hypersensitive C-reactive protein,hs-CRP)、白介素-6(interleukin-6,IL-6)、肿瘤坏死因子(tumor necrosis factor-α,TNF-α)、一氧化氮(nitric oxide,NO)及内皮素-1(endothelin-1,ET-1)水平的变化。结果:治疗前,两组血清TC、TG、LDL-C、HDL-C、hs-CRP、IL-6、TNF-α、NO及ET-1水平比较差异均无统计学意义(P0.05);治疗后,两组血清TC、TG、LDL-C、hs-CRP、IL-6、TNF-α及ET-1水平与本组治疗前相比均显著性降低,且观察组治疗后血清TC、TG、LDL-C、hs-CRP、IL-6、TNF-α及ET-1的水平均显著低于对照组(P0.05);两组血清HDL-C、NO水平与治疗前相比均显著性升高(P0.05),且观察组治疗后的血清HDL-C、NO水平显著高于对照组(P0.05)。结论:阿托伐他汀用于经PCI术治疗的老年ACS患者可显著减轻再灌注后的炎症反应,降低血脂水平并改善内皮功能,且大剂量阿托伐他汀的治疗效果明显优于小剂量治疗。     

阿托伐他汀对老年冠心病合并糖尿病患者的治疗效果及对血脂、尿酸水平的影响

目的:探讨阿托伐他汀对老年冠心病合并糖尿病患者的治疗效果及对血脂、尿酸水平的影响。方法:收集我院就诊的116例冠心病合并糖尿病患者,随机分为对照组和实验组,每组各58例。两组患者入院后均给予控制血糖、降血压等对症治疗。对照组患者给予阿司匹林肠溶片0.3~0.6g/次,3次/d,口服,氯吡格雷片2片/次,1次/d,口服,硝酸甘油0.25~0.5 g/次,3次/d,含服;实验组患者在对照组基础上给予阿托伐他汀片10~20 mg/次,1次/d,治疗连续4周,治疗期间根据患者情况及时调整药量。观察并比较两组患者治疗前后血清低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、甘油三酯(TG)、总胆固醇(TC)、尿酸(UA)、糖化血红蛋白(HbA1c)水平以及临床疗效。结果:与治疗前相比,两组患者治疗后的血清LDL-C、TG、TC、UA、Hb A1c水平均下降,HDL-C水平升高,差异具有统计学意义(P0.05);与对照组相比,实验组患者的LDL-C、TG、TC、UA、Hb A1c水平较低,HDL-C水平及临床治疗有效率均较高,差异均具有统计学意义(P0.05)。结论:阿托伐他汀能够有效降低老年冠心病合并糖尿病患者血糖、血脂以及尿酸水平,且临床治疗效果较好。     

Effects of Calcium Ions and of Calcium Channel Blockers on Galvanotaxis of Chlamydomonas reinhardtii

The effects of calcium ions and of the calcium channel blockers verapamil, diltiazem and nifedipine on galvanotaxis in Chlamydomonas have been investigated using a fully automated and computerized population system. Galvanotaxis is a function of the voltage applied to the cell population. However, the galvanotactic orientation also depends on the external calcium concentration. In a calcium-deprived nutrient medium which still contains 6 × 10^?7M calcium, galvanotactic orientation is about 20% of orientation at optimal calcium concentration of 10^?4 M at 9 V. The higher the external calcium concentration is, the lower is the voltage necessary for optimal galvanotactic orientation. The calcium channel blockers diltiazem and nifedipine likewise inhibit galvanotaxis of Chlamydomonas very specifically without impairing motility. Verapamil is effective, but also inhibits motility by causing detachment or shortening of the flagella. Nevertheless, inhibition of galvanotaxis by verapamil is not the only result of decreased motility, because the galvanotactic orientation is impaired to a greater extent than motility. The effectiveness of the three blockers tested in inhibiting galvanotaxis depends on the concentration and on the voltage applied. At 10^?5 M, verapamil causes maximal inhibition of galvanotaxis at 9 V. At increasing concentrations up to 10^?4 M, diltiazem inhibits galvanotaxis more strongly than the other blockers. If the voltage is varied at a constant blocker concentration of 2 × 10^?5 M, nifedipine causes maximal inhibition at 3 V–6 V, diltiazem at 9 V and verapamil above 12 V.     

钙指示剂的发展及其研究现状

钙指示剂常被用于细胞及细胞器钙信号的检测,是钙信号转导研究中必不可少的工具.目前的钙指示剂分两大类,包括化学钙指示剂,如Fura-2、Indo-1、Fluo-4等,和基因编码的钙指示蛋白如D1ER、GCaMP、CEPIA1er等.随着技术的发展及研究需求的不断提升,各版本的钙指示剂也在不断更新.本文对已有的钙指示剂进行了系统地梳理,详细介绍了目前应用最为广泛的钙指示剂,总结了现有钙指示剂的优缺点,并对可优化提升的部分进行了展望,旨在为钙指示剂研究的进一步发展提供一些思路.     

Ganglioside Function in Calcium Homeostasis and Signaling

Ganglioside function in eukaryotic cells encompasses a variety of modulatory interactions related to both development and mature cellular behavior. In relation to the nervous system this includes induction of neurite outgrowth and trophic/neuroprotective phenomena; more generally this applies to ganglioside effects on receptor function, adhesion reactions, and signal transduction mechanisms in neural and extraneural systems. Underlying many of these trophic effects are ganglioside-induced changes in cellular calcium, accomplished through modulation of Ca²⁺ influx channels, Ca²⁺ exchange proteins, and various Ca²⁺-dependent enzymes that are altered through association with gangliosides. A clear distinction needs to be drawn between intrinsic functions of gangliosides as naturally expressed by the cell and activities created by application of exogenous ganglioside(s) that may or may not reflect natural function. This review attempts to summarize findings in this area and point to possible future directions of research.     

天然产物中的钙离子拮抗剂

钙离子拮抗剂是一类广泛应用于心血管疾病以及其它多种疾病的药物。本文综述了来源于天然产物的钙离子拮抗剂。     

Calcium in plant defence-signalling pathways

In plant cells, the calcium ion is a ubiquitous intracellular second messenger involved in numerous signalling pathways. Variations in the cytosolic concentration of Ca2+ ([Ca2+]cyt) couple a large array of signals and responses. Here we concentrate on calcium signalling in plant defence responses, particularly on the generation of the calcium signal and downstream calcium-dependent events participating in the establishment of defence responses with special reference to calcium-binding proteins.     

钙稳态失衡与癌细胞抑制

细胞胞浆钙离子浓度必须处于严格的调控之中,钙稳态失调必将导致细胞严重损伤或死亡（凋亡或坏死）.综述了钙稳态失调在外界因素引起细胞死亡中的作用、直接钙稳态失调的细胞死亡效应、以及钙离子在细胞凋亡中的作用,并讨论了上述作用的机制,最后在总结基础上提出了一种抑癌新途径——选择性引发癌细胞钙稳态失衡.     

Calcium and diacylglycerol control of secretion

Measurements of intracellular Ca²⁺ in adrenal medullary cells suggest that a transient rise in Ca²⁺ leads to a transient secretory response, the rise in Ca²⁺ being brought about by an influx through voltage-sensitive Ca channels which subsequently inactivate. The level of Ca²⁺ observed is much smaller than the Ca²⁺ needed to trigger secretion when introduced directly into the cell. The discrepancy is removed by the presence of diacylglycerot, which increases the sensitivity of the secretory process to Ca²⁺. The site of action of Ca²⁺ and diacylglycerol is probably protein kinase C, and tile different secretory responses to increases of Ca²⁺ and diacylglycerol can be modelled in terms of a preferential order of binding of these two substrates to the enzyme. ATP is needed for secretion: one role is possibly to confer stability to the secretory apparatus; another may involve phosphorylation of some key protein. The kinetics of secretion suggest that if Ca²⁺ regulates phosphorylation or dephosphorylation, then it is therate of change of phosphorylation that controls secretion rather than theextent of phosphorylation or dephosphorylation. Guanine nucleotide-binding proteins may play a role not only at the level of signal transduction coupling, but also at or near the site of exocytosis, and the mechanism by which some Botulinum toxins inhibit secretion may be associated with these proteins.     

Tree Species Effects on Calcium Cycling: The Role of Calcium Uptake in Deep Soils

Soil acidity and calcium (Ca) availability in the surface soil differ substantially beneath sugar maple (Acer saccharum) and eastern hemlock (Tsuga canadensis) trees in a mixed forest in northwestern Connecticut. We determined the effect of pumping of Ca from deep soil (rooting zone below 20-cm mineral soil) to explain the higher available Ca content in the surface soil beneath sugar maple. We measured the atmospheric input of Ca with bulk deposition collectors and estimated Ca weathering and Ca mineralization in the surface soil (rooting zone above 20-cm mineral soil) from strontium isotope measurements and observed changes in exchangeable Ca in soils during field incubation. Calcium leaching at 20 cm was calculated by combining modeled hydrology with measured Ca soil solution concentrations at 20-cm depth. We measured root length distribution with depth beneath both tree species. Calcium leaching from the surface soil was much higher beneath sugar maple than hemlock and was positively related with the amount of Ca available in the surface soil. Calcium leaching from the surface soil beneath sugar maple was higher than the combined Ca input from atmospheric deposition and soil weathering. Without Ca uptake in the deep soil, surface soils are being depleted in Ca, especially beneath sugar maple. More organically bound Ca was mineralized beneath sugar maple than beneath hemlock. A relatively small part of this Ca release was leached below the surface soil, suggesting that, beneath both tree species, most of the Ca cycling is occurring in the surface soil. Sugar maple had more fine roots in the deep soil than hemlock and a greater potential to absorb Ca in the deep soil. With a simple model, we showed that a relatively small amount of Ca uptake in the deep soil beneath sugar maple is able to sustain high amounts of available Ca in the surface soil. Received 20 June 2001; accepted 6 December 2001.     

Modeling the Calcium Signaling in Stomatal Guard Cells under the Action of Abscisic Acid

A theoretical model of calcium signaling is presented that simulates oscillations of cytoplasmic calcium concentration ([Ca²⁺]_cyt) in stomatal guard cells under the action of abscisic acid. The model is based on the kinetics of inositol 1,4,5-trisphosphate-sensitive calcium channels of endoplasmic reticulum and cyclic ADP-ribose-sensitive calcium channels of the tonoplast. The operation of two energy-dependent pumps—the Ca²⁺-ATPase of the endoplasmic reticulum and the Ca²⁺/H⁺ antiporter of the tonoplast—is also included in the model. It is shown that the removal of excessive Ca²⁺ from the cytoplasm by the tonoplast Ca²⁺/H⁺ antiporter is the main factor accounting for generation of [Ca²⁺]_cyt oscillations at a wide range of ABA concentrations (0.01–1 M). The long period of [Ca²⁺]_cyt oscillations in plant cells is explained by a slow release from inhibition of inositol 1,4,5-trisphosphate-gated calcium channels.     

Calcium Sequestering Ability of Mitochondria Modulates Influx of Calcium through Glutamate Receptor Channel

The excitotoxicity of glutamate is believed to be mediated by sustained increase in the cytosolic Ca²⁺ concentration. Mitochondria play a vital role in buffering the cytosolic calcium overload in stimulated neurons. Here we have studied the glutamate induced Ca²⁺ signals in cortical brain slices under physiological conditions and the conditions that modify the mitochondrial functions. Exposure of slices to glutamate caused a rapid increase in [Ca²⁺]_i followed by a slow and persistently rising phase. The rapid increase in [Ca²⁺]_i was mainly due to influx of Ca²⁺ through the N-methyl-D-aspartate (NMDA) receptor channels. Glutamate stimulation in the absence of Ca²⁺ in the extracellular medium elicited a small transient rise in [Ca²⁺]_i which can be attributed to the mobilization of Ca²⁺ from IP₃ sensitive endoplasmic reticulum pools consequent to activation of metabotropic glutamate receptors. The glutamate induced Ca²⁺ influx was accompanied by depolarization of the mitochondrial membrane, which was inhibited by ruthenium red, the blocker of mitochondrial Ca²⁺ uniporter. These results imply that mitochondria sequester the Ca²⁺ loaded into the cytosol by glutamate stimulation. Persistent depolarization of mitochondrial membrane observed in presence of extracellular Ca²⁺ caused permeability transition and released the sequestered Ca²⁺ which is manifested as slow rise in [Ca²⁺]_i. Protonophore carbonyl cyanide m-chlorophenyl-hydrazone (CCCP) depolarized the mitochondrial membrane and enhanced the glutamate induced [Ca²⁺]_i response. Contrary to this, treatment of slices with mitochondrial inhibitor oligomycin or ruthenium red markedly reduced the [Ca²⁺]_i response. Combined treatment with oligomycin and rotenone further diminished the [Ca²⁺]_i response and also abolished the CCCP mediated rise in [Ca²⁺]_i. However, rotenone alone had no effect on glutamate induced [Ca²⁺]_i response. These changes in glutamate-induced [Ca²⁺]_i response could not be explained on the basis of deficient mitochondrial Ca²⁺ sequestration or ATP dependent Ca²⁺ buffering. The mitochondrial inhibitors reduced the cellular ATP/ADP ratio, however, this would have restrained the ATP dependent Ca²⁺ buffering processes leading to elevation of [Ca²⁺]_i. In contrast our results showed repression of Ca²⁺ signal except in case of CCCP which drastically reduced the ATP/ADP ratio. It was inferred that, under the conditions that hamper the Ca²⁺ sequestering ability of mitochondria, the glutamate induced Ca²⁺ influx could be impeded. To validate this, influx of Mn²⁺ through ionotropic glutamate receptor channel was monitored by measuring the quenching of Fura-2 fluorescence. Treatment of slices with oligomycin and rotenone prior to glutamate exposure conspicuously reduced the rate of glutamate induced fluorescence quenching as compared to untreated slices. Thus our data establish that the functional status of mitochondria can modify the activity of ionotropic glutamate receptor and suggest that blockade of mitochondrial Ca²⁺ sequestration may desensitize the NMDA receptor operated channel.