Up-regulated L-type high voltage-gated calcium channels cause increase in diazepam binding inhibitor induced by sustained morphine exposure in mouse cerebrocortical neurons.
Up-regulated L-type high voltage-gated calcium channels cause increase in diazepam binding inhibitor induced by sustained morphine exposure in mouse cerebrocortical neurons.
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DOI：
10.1016/j.lfs.2006.08.036
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发表时间：
2006-12
期刊：
影响因子：
6.1
通讯作者：
M. Shibasaki;M. Katsura;A. Tsujimura;S. Ohkuma
中科院分区：
文献类型：
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作者：
M. Shibasaki;M. Katsura;A. Tsujimura;S. Ohkuma
研究了吗啡持续暴露后小鼠脑皮质神经元地西泮结合抑制剂（DBI） mRNA表达增加的机制。吗啡（0.3 μM）持续暴露3 d后，纳洛酮和硝苯地平可完全消除DBI和mRNA表达的升高，ω-agatoxin VIA和ω- concontoxin GIVA则不能。[3H]地尔硫卓与吗啡处理神经元颗粒组分结合的增加是由于Bmaxvalue增加而Kdvalue没有变化。Western blot分析显示，α1C、α1D和α2/δ1亚基表达增加，β4亚基表达减少，而N-和P/ q型HVCC亚基表达不变。这些结果表明，吗啡诱导的DBI mRNA表达增加是通过上调l型hvcc介导的Ca2+进入增加。
Mechanisms of increase in diazepam binding inhibitor (DBI) mRNA expression in mouse cerebrocortical neurons after sustained morphine exposure were investigated. Increases in DBI and its mRNA expressions induced by sustained morphine (0.3 μM) exposure for 3 days were completely abolished by naloxone and nifedipine, but not by ω-agatoxin VIA and ω-conotoxin GIVA. Increase in [3H]diltiazem binding to the particulate fractions from the morphine-treated neurons was due to increased Bmaxvalue with no changes in Kdvalue. Western blot analysis on l-type high voltage-gated calcium channel (HVCC) subunits revealed the increased expressions of α1C, α1D, and α2/δ1 subunits and decreased of β4 subunit expression, whereas expression of N- and P/Q-type HVCC subunits was not changed. These results indicate that morphine-induced increase in DBI mRNA expression is mediated via increased Ca2+entry through up-regulated l-type HVCCs.