期刊文献+

海马CA_1区锥体细胞内钙离子释放与突触传递的可塑性 被引量:2

THE RELATIONSHIP BETWEEN CALCIUM RELEASE FROM CA_1 PYRAMIDAL NEURON INDUCED BY SYNAPTIC STIMULATION AND PLASTICITY OF SYNAPTIC TRANSMISSION IN HIPPOCAMPUS
下载PDF
导出
摘要 为分析海马CA1区锥体细胞内钙离子释放与突触传递长时程增强以及长时程抑制的关系,采用全细胞膜片钳和细胞内钙成像技术,观察了不同参数的突触前刺激引起大鼠海马锥体细胞内钙离子释放的状况。结果为:100Hz、50Hz、20Hz频率,分别用50、25、15、10、5脉冲的突触前刺激均可引起锥体细胞内钙的释放,10脉冲以上的刺激引起细胞内钙释放的成功率为100%,而5脉冲的刺激引起细胞内钙的释放率为57%。100 Hz 3脉冲的刺激可引起少数锥体细胞内钙释放,而5 Hz各脉冲的刺激均不能引起锥体细胞内钙的释放。结果提示,长时程抑制时细胞内钙的升高并非来自于细胞内钙库的钙释放;引起长时程增强的刺激参数与引起锥体细胞内钙释放的参数相似。本文又分析了两者的异同处。 Whole cell patch clamp recording and calcium image technique were used to analyze the relationship between calcium release from CA1 pyramidal neuron and the plasticity of synaptic transmission in hippocampus. We observed condition of calcium release from CA1 pyramidal neuron induced by synaptic stimulation. The results showed that stimulating frequency of 100, 50, and 20 Hz when 50, 25, 15, 10 and 5 pulses were used, respectively, could evoke the calcium release from internal store of the neuron. Stimulating frequency of 5 Hz could not induce the release. When a number of stimulating pulses of 10 or higher than 10 were used, the success rate of calcium release from the internal store was 100%. But when the number of stimulating pulses of 5 was used, the rate of calcium release was 57%. The results indicate that the calcium increase in pyramidal neuron in long-term depression is not released from the internal calcium store; the stimulating protocol that induced calcium release is similar to the protocol that generated long-term potentiation, we have analyzed the similarity and difference between the two phenomena.
作者 周苏娅 夏强
出处 《神经解剖学杂志》 CAS CSCD 北大核心 2003年第1期11-16,共6页 Chinese Journal of Neuroanatomy
基金 国家自然科学基金(No.39770252)资助项目
关键词 海马CA1区 锥体细胞 钙离子 释放 突触 传递 calcium release, long-term potentiation, long-term depression, CA1 pyramidal neuron, hippocampus, rat
  • 相关文献

参考文献13

  • 1[1]Bliss T, Lomo T. Long-lasting potentiation of synaptic transmission in the dentate area of the anesthetized rabbit following stimulation of the perforant path. J Physiol(Lond), 1973,232:331 ~356
  • 2[2]Bliss T. Collingridge GL. A synaptic model of memory: longterm potentiation in the hippocampus. Nature, 1993,361 :31~39
  • 3[3]Nakamura T, Barbara J, Nakamura K, et al. Synergistic release of Ca2+ from InsP3-sensitive stores evoked by synaptic activation of mGlu receptors paired with backpropagating action potentials. Neuron, 1999,24:727~ 737
  • 4[4]Yang SN, Tang YG, Zucker RS. Selective induction of LTP and LTD by postsynaptic [Ca2+ ]i elevation. J Neurophysiol,1999,81:781~787
  • 5[5]Connor JA, Petrozzino J, Pozzo Miller LD, et al. Calcium signals in long-term potentiation and long-term depression. Can J Physiol Pharmacol, 1999,77: 722~ 734
  • 6[6]Sakmann B, Stuart G. Patch-pipette recordings from the soma,dendrites, and axon of neurons in brain slices. In single channel recording, 2nd Ed. Sakmann B and Neher E. eds. New York: Plenum, 1995,pp199~211
  • 7[7]Lechleiter J, Girard S, Peralta E, et al. Spiral calcium wave propagation and annihilation in Xenopus laevis oocytes. Science, 1991,252:123~126
  • 8[8]Marchant J, Callamaras N, Parker I. Initiation of IP3-mediated Ca2+ waves in Xenopus oocytes. EMBO J, 1999, 18:5285~5299
  • 9[9]Madison DV, Malenka RC, Nicoll RA. Mechanisms underlying long-term potentiation of synaptic transmission. Annu Rev Neurosci, 1991,14:379~397
  • 10[10]Dunwiddie T, Lynch G. Long-term potentiation and depression of synaptic responses in the rat hippocampus: localization and frequency dependency. J Physiol (Lond), 1978,276: 353 ~367

同被引文献24

  • 1耿芳芳,许伟,郭利伟,樊海新,吴金节,李治忠,王希春.复合吸附剂对AFB_1和DON暴露鸡血清生化指标的影响[J].中国兽医学报,2015,35(3):507-511. 被引量:8
  • 2彭双清,杨进生.镰刀菌毒素脱氧雪腐镰刀菌烯醇对心肌细胞Ca^(2+)通道的阻滞作用[J].中国预防医学杂志,2004,5(4):241-243. 被引量:13
  • 3Linstedt A D, Kelly R B. Molecular architecture of the nerve terminal. Curt Opin Neurobiol, 1991, 1 (3): 382-387.
  • 4Lipton S A, Kater S B. Neurotransmitter regulation of neuronal outgrowth, plasticity and survival. Trends Neurosci, 1989, 12 (7):265-270.
  • 5Dawson V L, Dawson T M. Physiological and toxicological actions of nitric oxide in the central nervous system. Adv Pharmacol, 1995,34:323-342.
  • 6Muller F, Koch K W. Calcium-binding proteins and nitric oxide in retinal function and disease. Acta Anatomica, 1998, 162 (2-3):142-150.
  • 7Sattler R, Xiong Z, Lu W Y, et al. Specific coupling of NMDA receptor activation to nitric oxide neurotoxicity by PSD-95 protein.Science, 1999, 284 (5421): 1845-1848.
  • 8Lentile R, Pedale S, C6noprelli T, et al. Intracellular polyamine levels are involved in NMDA-evoked nitric oxide production in chick retina cells. J Neurochem, 1999, 72 (4): 1744-1749.
  • 9Vidwans A S, Kim S, Coffin D O, et al. Analysis of the neuroprotective effects of various nitric oxide donor compounds in murine mixed cortical cell culture. J Neurochem, 1999, 72(5):1843-1852.
  • 10Kim W K, Choi Y B, Rayudu V P, et al. Attenuation of NMDA receptor activity and neurotoxicity by nitroxyl anion, NO-. Neuron,1999, 24 (2): 461-469.

引证文献2

二级引证文献5

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部