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孤立的N-甲基-D-天冬氨酸受体介导的突触反应同时表现出长时程增强和长时程抑制。

Isolated NMDA receptor-mediated synaptic responses express both LTP and LTD.

作者信息

Xie X, Berger T W, Barrionuevo G

机构信息

Department of Behavioral Neuroscience, University of Pittsburgh, Pennsylvania 15260.

出版信息

J Neurophysiol. 1992 Apr;67(4):1009-13. doi: 10.1152/jn.1992.67.4.1009.

Abstract
  1. The possibility of use-dependent, long-lasting modifications of pharmacologically isolated N-methyl-D-aspartate (NMDA) receptor-mediated synaptic transmission was examined by intracellular recordings from granule cells of the hippocampal dentate gyrus in vitro. In the presence of the non-NMDA receptor antagonist 6-cyano-7-nitroquinaxaline-2,3-dione (CNQX, 10 microM) robust, long-term potentiation (LTP) of NMDA receptor-mediated synaptic potentials was induced by brief, high (50 Hz) and lower (10 Hz) frequency tetanic stimuli of glutamatergic afferents (60 +/- 6%, n = 8, P less than 0.001 and 43 +/- 12%, n = 3, P less than 0.05, respectively). 2. Hyperpolarization of granule cell membrane potential to -100 mV during 50-Hz tetanic stimuli reversibly blocked the induction of LTP (-6 +/- 2%, n = 6, P greater than 0.05) indicating that simultaneous activation of pre- and postsynaptic elements is a prerequisite for potentiation of NMDA receptor-mediated synaptic transmission. In contrast, hyperpolarization of the granule cell membrane potential to -100 mV during 10-Hz tetanic stimuli resulted in long-term depression (LTD) of NMDA receptor-mediated synaptic potentials (-34 +/- 8%, n = 8, P less than 0.01). 3. We also studied the role of [Ca2+]i in the induction of LTP and LTD of NMDA receptor-mediated synaptic responses. Before tetanization, [Ca2+]i was buffered by iontophoretic injections of bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA). BAPTA completely blocked the induction of LTP (3 +/- 5%, n = 13) and partially blocked LTD (-14.8 +/- 6%, n = 10).(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 通过对体外培养的海马齿状回颗粒细胞进行细胞内记录,研究了药理学分离的N-甲基-D-天冬氨酸(NMDA)受体介导的突触传递发生使用依赖性、长期修饰的可能性。在非NMDA受体拮抗剂6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX,10微摩尔)存在的情况下,通过对谷氨酸能传入神经进行短暂、高频(50赫兹)和低频(10赫兹)强直刺激,可诱导NMDA受体介导的突触电位产生强大的长期增强(LTP)(分别为60±6%,n = 8,P<0.001和43±12%,n = 3,P<0.05)。2. 在50赫兹强直刺激期间,将颗粒细胞膜电位超极化至-100毫伏可可逆地阻断LTP的诱导(-6±2%,n = 6,P>0.05),这表明突触前和突触后元件的同时激活是NMDA受体介导的突触传递增强的先决条件。相比之下,在10赫兹强直刺激期间,将颗粒细胞膜电位超极化至-100毫伏会导致NMDA受体介导的突触电位出现长期抑制(LTD)(-34±8%,n = 8,P<0.01)。3. 我们还研究了细胞内钙离子浓度[Ca2+]i在NMDA受体介导的突触反应LTP和LTD诱导过程中的作用。在强直刺激前,通过离子电泳注射双(邻氨基苯氧基)-N,N,N',N'-四乙酸(BAPTA)来缓冲[Ca2+]i。BAPTA完全阻断了LTP的诱导(3±5%,n = 13),并部分阻断了LTD(-14.8±6%,n = 10)。(摘要截短于250字)

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