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在海马体CA1区神经元中,N-甲基-D-天冬氨酸(NMDA)受体的氧化还原状态决定了由NMDA受体而非α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体所表达的长时程增强效应。

In CA1 hippocampal neurons, the redox state of NMDA receptors determines LTP expressed by NMDA but not by AMPA receptors.

作者信息

Gozlan H, Khazipov R, Diabira D, Ben-Ari Y

机构信息

Institut National de la Santé et de la Recherche Médicale Unité 29, Paris, France.

出版信息

J Neurophysiol. 1995 Jun;73(6):2612-7. doi: 10.1152/jn.1995.73.6.2612.

DOI:10.1152/jn.1995.73.6.2612
PMID:7666170
Abstract
  1. Using extracellular recording techniques in the CA1 region of the rat hippocampus, we have evaluated the effects of the redox reagents 5,5O-dithiobis-2-nitrobenzoic acid (DTNB) and tris (carboxyethyl) phosphine (TCEP) on long-term potentiation (LTP) expressed by alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptors. In physiological conditions a high-frequency stimulation (HFS) of Schaffer collateral-commissural fibers induced a LTP expressed by a persistent increase (73 +/- 13%, mean +/- SE, n = 8/10) of AMPA field potentials (LTPA). In the presence of 10 microM of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and reduced concentration of Mg2+ (0.1 mM) to boost NMDA receptors, the HFS induced LTP of NMDA field potentials (LTPN; 62 +/- 11%, n = 8/10). 2. The thiol-oxidizing reagent DTNB (200 microM) reduced, by 46 +/- 5% (n = 24), NMDA-receptor field potentials (NMDA-FP), and this effect could not be reversed by extensive washing. The disulfide-reducing agent TCEP (200 microM) slightly increased AMPA-FP and reversed the DTNB-induced inhibition of NMDA-FP. 3. DTNB (200 microM, 10 min), and TCEP (200 microM, 20 min), had no effect on AMPA-FP (98 +/- 3% and 101 +/- 5%, respectively, n = 12). 4. DTNB (200 microM, 15 min) did not prevent the induction or expression of LTPA (-12 and -5%, respectively, n = 8/8). Similar results were observed with TCEP (200 microM, 20 min).(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
  1. 我们运用细胞外记录技术,在大鼠海马体的CA1区域评估了氧化还原试剂5,5'-二硫代双(2-硝基苯甲酸)(DTNB)和三(羧乙基)膦(TCEP)对由α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)和N-甲基-D-天冬氨酸(NMDA)受体所表达的长时程增强(LTP)的影响。在生理条件下,对海马联合纤维进行高频刺激(HFS)可诱导AMPA场电位持续增加(73±13%,平均值±标准误,n = 8/10)所表达的LTP(AMPA-LTP)。在存在10微摩尔6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)并降低镁离子浓度(0.1毫摩尔)以增强NMDA受体的情况下,HFS可诱导NMDA场电位的LTP(NMDA-LTP;62±11%,n = 8/10)。2. 硫醇氧化试剂DTNB(200微摩尔)使NMDA受体场电位(NMDA-FP)降低了46±5%(n = 24),且这种效应无法通过大量冲洗逆转。二硫键还原试剂TCEP(200微摩尔)使AMPA-FP略有增加,并逆转了DTNB对NMDA-FP的抑制作用。3. DTNB(200微摩尔,1分钟)和TCEP(200微摩尔,20分钟)对AMPA-FP均无影响(分别为98±3%和101±5%,n = 12)。4. DTNB(200微摩尔,15分钟)并未阻止AMPA-LTP的诱导或表达(分别为-12%和-5%,n = 8/8)。TCEP(200微摩尔,20分钟)也得到了类似结果。(摘要截选至250字)

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In CA1 hippocampal neurons, the redox state of NMDA receptors determines LTP expressed by NMDA but not by AMPA receptors.在海马体CA1区神经元中,N-甲基-D-天冬氨酸(NMDA)受体的氧化还原状态决定了由NMDA受体而非α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)受体所表达的长时程增强效应。
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[NMDA receptor and long-term potentiation].[NMDA受体与长时程增强]
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