Neuro-protective effects of CNTF on hippocampal neurons via an unknown signal transduction pathway

Stress is one of the leading contributing factors for psychosomatic diseases of modern society. Prolonged or strong stress may cause more release of glutamic acid (Glu) transmitter from hippocampal neurons. As most hippocampal neurons are glutaminergic ne…     

β-Adrenergic activation enhances NMDA-induced current in pyramidal cells of the basolateral nucleus of amygdala

NMDA receptor （NMDA-R） in the amygdala complex is critical for both long-term potentiation （LTP） and formation of conditioned fear memory. It is reported that activation of β-adrenoceptors （β-AR） in the amygdala facilitates LTP and enhances memory consolidation. The present study examined the regulatory effect of β-AR activation on NMDA-R mediated current in pyramidal cells of the basolateral nucleus of amygdala （BLA）, using whole-cell recording technique. Bath application of the β-AR agonist isoproterenol enhanced NMDA-induced current, and this facilitatory effect was blocked by co-administered propranolol, a β-AR antagonist. The facilitatory effect of isoproterenol on NMDA-induced current could not be induced when the protein kinase A （PKA） inhibitor Rp-cAMPs was added in electrode internal solution.The present results suggest that β-AR activation in the BLA could modulate NMDA-R activity directly and positively, probably via PKA.     

Baclofen对大鼠新鲜分离DRG神经元GABA和NMDA激活电流的抑制作用

用全细胞膜片箝技术在大鼠新鲜分离的背根神经节 (DRG)细胞上观察到baclofen对GABA和NMDA激活电流有调制作用。单独给予DRG细胞baclofen (1～ 10 0 μmol/L)未记录到可测的电流改变 ,但预加baclofen对GABA和NMDA激活电流具有明显的抑制作用 ,且呈剂量依赖性。 10 0 μmol/Lbaclofen对GABA和NMDA激活电流分别抑制(5 1.2± 10 .9) % (X±SE ,n=8,P <0 .0 1)和 (6 4 .1± 2 1.1) % (X±SE ,n=6 ,P <0 .0 1) ,此抑制作用是可逆的 ,可被GABAB 受体拮抗剂saclofen(10 0 μmol/L ) 所取消 (n =4 )。     

Aniracetam对小白鼠被动回避反应的影响

本文建立了被动回避行为的实验模型，并用此模型观察了Ａｎｉｒａｃｅｔａｍ对小白鼠被动回避行为的建立，保持和消退的影响，结果表明Ａｎｉｒａｃｅｔａｍ对被动回避行为的建立没有明显的影响，在行为的保持和消退过程中，则有明显的延缓作用，Ａｎｉｒａｃｅｔａｍ对正常动物记忆的保存有效。     

东亚钳蝎提取物对癫痫小鼠NMDA受体的抑制作用

研究BmKE的抗癫痫作用及其机制。观察戊四氮(PTZ)致癫痫模型小鼠,丙戊酸钠(VAP)对照治疗组和BmKE高(BmKEH)、中(BmKEM)、低(BmKEL)剂量治疗组小鼠癫痫发作的潜伏期;应用同位素3H标记MK-801检测小鼠大脑皮层兴奋性N-甲基-D-门冬氨酸受体(NMDAR)结合活性。结果发现,VAP和BmKEM能显著延长PTZ致癫痫小鼠的发作潜伏期(p<0.05)。PTZ致癫痫小鼠大脑皮层的NMDAR结合活性比正常对照组升高了18%(p<0.05),经治疗的VAP和BmKEL组小鼠大脑皮层NMDAR结合活性明显降低(p<0.05),分别降低了14%和13%,BmKEM和BmKEH均显著降低癫痫小鼠大脑皮层NMDAR结合活性(p<0.001),分别降低了49%和53%。BmKE对大脑皮层的兴奋性NMDAR的抑制作用呈剂量相关性。     

NMDA受体概述及其在学习记忆中的作用

NMDA受体是由多亚基构成的异聚体,是最重要的谷氨酸受体之一,主要分布在中枢系统中.NMDA受体有多个调节位点,能被谷氨酸、甘氨酸、Ca2+、酶等多种因素影响.NMDA受体介导的Ca2+内流广泛地参与多种生理作用,其引发的长时程增强作用而对学习记忆有极其重要的作用.     

缺锌以生长大鼠记忆的影响及有关机制的研究

采用Wistar大鼠建立缺锌模型，观察了缺锌对大鼠记忆能力及其脑组织中游离脂肪酸，5－羟色胺（5－HT），乙酰胆碱，一氧化氮（NO）合酶活性，生长抑素和N－甲基－D－天门冬氨酸受体（NMDA－R）的影响，结果表明，缺锌明显降低大鼠记忆能力，同时使大鼠脑组织乙酰胆碱，NO合酶活性，生长抑素和NMDA受体含量显著降低，而使脂肪酸和5－HT含量显著升高，此结果提示，缺锌引起记忆功能的降低可能与脑组织中这此功能物质的变化有关。     

Molecular mechanisms of glutamate-dependent neurodegeneration in ischemia and traumatic brain injury

Stroke and neurotrauma mediate neuronal death through a series of events that involve multiple interdependent molecular pathways. It has been suggested that these pathways are triggered following elevations in extracellular excitatory amino acids, primarily glutamate [1]. This report outlines mechanisms involving glutamate-mediated excitotoxicity with specific focus on (i) the role of Ca²⁺ in neurotoxicity, (ii) The concept of source specificity of neurotoxicity, (iii) the role of the ionotropic N-methyl-D-aspartate (NMDA)-subtype glutamate receptor and its associated submembrane molecules that may give rise to signaling specificity in excitotoxicity and (iv) the role of glutamate-mediated free-radical generation and associated cell death pathways. We also highlight a novel, peptide-based approach for uncoupling NMDA receptors from excitotoxicity in the rat central nervous system subjected to focal ischemia, thereby reducing stroke infarct volume and improving neurological functioning.Received 11 August 2003; received after revision 15 September 2003; accepted 17 September 2003