Differential activation of brain-derived neurotrophic factor gene promoters I and III by Ca2+ signals evoked via L-type voltage-dependent and N-methyl-D-aspartate receptor Ca2+ channels

被引:119
作者
Tabuchi, A
Nakaoka, R
Amano, K
Yukimine, M
Andoh, T
Kuraishi, Y
Tsuda, M
机构
[1] Toyama Med & Pharmaceut Univ, Fac Pharmaceut Sci, Dept Biol Chem, Toyama 9300194, Japan
[2] Toyama Med & Pharmaceut Univ, Fac Pharmaceut Sci, Dept Appl Pharmacol, Toyama 9300194, Japan
[3] Japan Sci & Technol Corp, Core Res Evolut Sci & Technol, Tokyo 1500002, Japan
关键词
D O I
10.1074/jbc.M909538199
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Although the brain-derived neurotrophic factor (BDNF) gene is activated by the intracellular Ca2+ signals evoked via Ca2+ influx into neurons, little is known about how the activation of alternative BDNF gene promoters is controlled by the Ca2+ signals evoked via N-methyl-D-aspartate receptors (NMDA-R) and L-type voltage-dependent Ca2+ channels (L-VDCC), There is a critical range in the membrane depolarization caused by high K+ concentrations (25-50 mM KCI) for effective BDNF mRNA expression and transcriptional activation of BDNF gene promoters I and III (BDNF-PI and -PIII, respectively) in rat cortical culture. The increase in BDNF mRNA expression induced at high K+ was repressed not only by nicardipine, an antagonist for L-VDCC, but also by DL-amino-5-phosphonovalerate, an antagonist for NMDA-R, which was supported by the effects of antagonists on the Ca2+ influx. Although the promoter activations at 25 and 50 mM KCI were different, BDNF-PIII was activated by either the Ca2+ influx through NMDA-R or L-VDCC, whereas BDNF-PI was predominantly by the Ca2+ influx through L-VDCC. Direct stimulation of NMDA-R supported the activation of BDNF-PIII but not that of BDNF-PI, Thus, the alternative BDNF gene promoters responded differently to the intracellular Ca2+ signals evoked via NMDA-R and L-VDCC.
引用
收藏
页码:17269 / 17275
页数:7
相关论文
共 25 条
  • [1] Molecular determinants for subcellular localization of PSD-95 with an interacting K+ channel
    Arnold, DB
    Clapham, DE
    [J]. NEURON, 1999, 23 (01) : 149 - 157
  • [2] Regulation of gene expression by alternative promoters
    Ayoubi, TAY
    VanDeVen, WJM
    [J]. FASEB JOURNAL, 1996, 10 (04) : 453 - 460
  • [3] REGULATION OF GENE-EXPRESSION IN HIPPOCAMPAL-NEURONS BY DISTINCT CALCIUM SIGNALING PATHWAYS
    BADING, H
    GINTY, DD
    GREENBERG, ME
    [J]. SCIENCE, 1993, 260 (5105) : 181 - 186
  • [4] Berman FW, 1997, J NEUROCHEM, V69, P693
  • [5] CREB phosphorylation and dephosphorylation: A Ca2(+)- and stimulus duration-dependent switch for hippocampal gene expression
    Bito, H
    Deisseroth, K
    Tsien, RW
    [J]. CELL, 1996, 87 (07) : 1203 - 1214
  • [6] Bruns D, 1997, J NEUROSCI, V17, P1898
  • [7] Regulation of adenylyl cyclase by membrane potential
    Cooper, DMF
    Schell, MJ
    Thorn, P
    Irvine, RF
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (42) : 27703 - 27707
  • [8] Coactivation of secretogranin-II and BDNF genes mediated by calcium signals in mouse cerebellar granule cells
    Fujita, Y
    Katagi, J
    Tabuchi, A
    Tsuchiya, T
    Tsuda, M
    [J]. MOLECULAR BRAIN RESEARCH, 1999, 63 (02): : 316 - 324
  • [9] CALCIUM SIGNALING IN NEURONS - MOLECULAR MECHANISMS AND CELLULAR CONSEQUENCES
    GHOSH, A
    GREENBERG, ME
    [J]. SCIENCE, 1995, 268 (5208) : 239 - 247
  • [10] Control of recruitment and transcription-activating function of CBP determines gene regulation by NMDA receptors and L-type calcium channels
    Hardingham, GE
    Chawla, S
    Cruzalegui, FH
    Bading, H
    [J]. NEURON, 1999, 22 (04) : 789 - 798