首页> 外文期刊>Life sciences >EVIDENCE FOR DECLINE IN INTRACELLULAR CALCIUM BUFFERING IN ADRENERGIC NERVES OF AGED RATS
【24h】

EVIDENCE FOR DECLINE IN INTRACELLULAR CALCIUM BUFFERING IN ADRENERGIC NERVES OF AGED RATS

机译:衰老大鼠肾上腺神经细胞内钙离子摄取下降的证据

获取原文
获取原文并翻译 | 示例
           

摘要

Age-related alterations in neuronal intracellular calcium regulation and neurotransmitter release have been widely reported. We have investigated the impact of age on neurotransmitter release and intracellular calcium buffering in adrenergic nerve endings of the isolated rat tail artery and on intracellular calcium in acutely dissociated cells from the superior cervical ganglion. Advancing age, from 6 to 27 months, resulted in significantly increased stimulation-evoked norepinephrine release from the isolated rat tail artery, an effect which persisted when neuronal and extraneuronal uptake were blocked with cocaine and deoxycorticosterone and presynaptic alpha adrenergic receptors were blocked with idazoxan. Alterations in extracellular calcium had significant effects on stimulation-evoked norepinephrine release, but these were much more marked in old, compared to young, arteries. Blockade of mitochondrial calcium accumulation with dinitrophenol had no significant effect on stimulation-evoked norepinephrine release from 6-month-old arteries, but in 20-month-old arteries, treatment with dinitrophenol resulted in a substantial increase in stimulation-evoked norepinephrine release. However, when extracellular calcium was increased to 5 mM in 6 month-old-arteries, then addition of dinitrophenol resulted in an increase in stimulation-evoked norepinephrine release. Measurement of intracellular calcium in acutely dissociated superior cervical ganglion cells using fura-2 revealed substantial age-related differences. Peak calcium transients in 20-month-old ganglion cells depolarized with 68 mM K+ were substantially higher than in 6-month-old cells. Together these findings support the hypothesis that in adrenergic nerves advancing age results in a disruption of intracellular calcium buffering leading to higher levels of intracellular calcium and increased transmitter release. [References: 23]
机译:广泛报道了神经元细胞内钙调节和神经递质释放的年龄相关变化。我们研究了年龄对离体大鼠尾动脉的肾上腺素能神经末梢神经递质释放和细胞内钙缓冲作用以及上颈神经节急性离解细胞中细胞内钙的影响。年龄从6个月提高到27个月,导致离体大鼠尾动脉的刺激诱发的去甲肾上腺素释放显着增加,当可卡因阻止脱氧神经皮质和神经元摄取,脱氧皮质酮和突触前α肾上腺素受体被咪唑烷抑制时,这种作用持续存在。细胞外钙的改变对刺激诱发的去甲肾上腺素释放有显着影响,但与年轻的动脉相比,这些在老年人中更为明显。用二硝基苯酚阻断线粒体钙积累对刺激诱发的去甲肾上腺素从6个月大的动脉释放没有显着影响,但在20个月大的动脉中,用二硝基苯酚治疗导致刺激诱发的去甲肾上腺素释放显着增加。但是,当在6个月大的动脉中将细胞外钙增加至5 mM时,则添加二硝基苯酚会导致刺激诱发的去甲肾上腺素释放增加。使用fura-2对急性分离的上颈神经节细胞中细胞内钙的测量显示出与年龄相关的实质性差异。用68 mM K +去极化的20个月大神经节细胞中的钙瞬变峰值明显高于6个月大神经节细胞。这些发现共同支持以下假设:在肾上腺能神经中,年龄增长会导致细胞内钙缓冲液的破坏,从而导致细胞内钙水平升高和递质释放增加。 [参考:23]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号