Ca2+ channel currents of cortical neurons from pure and mixed cultures

被引:2
|
作者
Zhou, Chen [1 ,2 ]
Yang, Aiying [3 ]
Chai, Zhen [1 ]
机构
[1] Peking Univ, Coll Life Sci, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China
[2] Hebei Univ, Coll Life Sci, Baoding 071002, Peoples R China
[3] Harbin Med Univ, Dept Cell Biol, Harbin 150086, Peoples R China
基金
中国国家自然科学基金;
关键词
Pure cultured neurons; Mixed cultured neurons; Ca2+ currents; Patch-clamp recording; SERUM-FREE CULTURE; CALCIUM-CHANNELS; NEUROTRANSMITTER RELEASE; HIPPOCAMPAL-NEURONS; CELL-DEATH;
D O I
10.1007/s10616-011-9405-2
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Voltage-gated Ca2+ channels (VGCCs) are key regulators of many neuronal functions, and involved in multiple central nervous system diseases. In the last 30 years, a large number of injury and disease models have been established based on cultured neurons. Culture with serum develops a mixture of neurons and glial cells, while culture without serum develops pure neurons. Both of these neuronal-culture methods are widely used. However, the properties of Ca2+ currents in neurons from these two cultures have not been compared. In this study, we cultured rat cortical neurons in serum-containing or free medium and then recorded the Ca2+ channel currents using patch-clamp technique. Our results showed that there were significant differences in the amplitude and activation properties of whole-cell Ca2+ channel currents, and of non-L-type Ca2+ channel currents between the neurons from these two culture systems. Our data suggested that the difference of whole-cell Ca2+ currents may result from the differences in non-L-type currents. Understanding of these properties will considerably advance studies of VGCCs in neurons from pure or mixed culture.
引用
收藏
页码:173 / 179
页数:7
相关论文
共 50 条
  • [41] Volatile anesthetics increase [Ca2+]i in cortical and hippocampal neurons
    Bickler, PE
    Kindler, C
    ANESTHESIOLOGY, 1998, 89 (3A) : U211 - U211
  • [42] Nicotinic modulation of Ca2+ oscillations in rat cortical neurons in vitro
    Wang, JianGang
    Wang, YaLi
    Guo, FangLi
    Feng, ZhiBo
    Wang, XiangFang
    Lu, ChengBiao
    AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2016, 310 (09): : C748 - C754
  • [43] Seletracetam (ucb 44212), a new pyrrolidone derivative, inhibits high-voltage-activated Ca2+ currents and intracellular [Ca2+] increase in rat cortical neurons in vitro
    Pisani, A
    Bonsi, P
    Martella, G
    Cuomo, D
    Klitgaard, H
    Margineanu, DG
    EPILEPSIA, 2005, 46 : 119 - 120
  • [44] Adrenoceptor-induced changes of intracellular K+ and Ca2+ in astrocytes and neurons in rat cortical primary cultures
    Muyderman, H
    Hansson, E
    Nilsson, M
    NEUROSCIENCE LETTERS, 1997, 238 (1-2) : 33 - 36
  • [45] Ca2+ channels that activate Ca2+-dependent K+ currents in neostriatal neurons
    Vilchis, C
    Bargas, J
    Ayala, GX
    Galván, E
    Galarraga, E
    NEUROSCIENCE, 2000, 95 (03) : 745 - 752
  • [46] Modulating Ca2+ clearance from neurons
    Thayer, SA
    Usachev, YM
    Pottorf, WJ
    FRONTIERS IN BIOSCIENCE-LANDMARK, 2002, 7 : D1255 - D1279
  • [47] Selectivities of a L- and N-type Ca2+ channel dual antagonist, cilnidipine, for the cardiac and the sympathetic Ca2+ channel currents
    Uneyama, H
    Takahara, A
    Yoshimoto, R
    Akaike, N
    JOURNAL OF HYPERTENSION, 1998, 16 : S242 - S242
  • [48] CORRELATION BETWEEN G PROTEIN-ACTIVATION AND REBLOCKING KINETICS OF CA2+ CHANNEL CURRENTS IN RAT SENSORY NEURONS
    LOPEZ, HS
    BROWN, AM
    NEURON, 1991, 7 (06) : 1061 - 1068
  • [49] A novel benzothiazine Ca2+ channel antagonist, semotiadil, inhibits cardiac L-type Ca2+ currents
    Koidl, B
    Miyawaki, N
    Tritthart, HA
    EUROPEAN JOURNAL OF PHARMACOLOGY, 1997, 322 (2-3) : 243 - 247
  • [50] Interleukin-1β downregulates the L-type Ca2+ channel activity by depressing the expression of channel protein in cortical neurons
    Zhou, C
    Tai, C
    Ye, HH
    Ren, X
    Chen, JG
    Wang, SQ
    Chai, Z
    JOURNAL OF CELLULAR PHYSIOLOGY, 2006, 206 (03) : 799 - 806