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首页> 外文学位 >Calcium ion influx and release in Aplysia bag cell neurons.
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Calcium ion influx and release in Aplysia bag cell neurons.

机译：钙离子流入和释放海藻袋细胞神经元。

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摘要

Intracellular Ca2+ is influenced by extracellular Ca2+ influx and release from internal stores. Depending on the initial influx, a range of responses can result. To better understand the processes surrounding Ca2+ handling, I examined intracellular Ca2+ following receptor-operated or voltage-gated Ca 2+ influx in bag cell neurons of the marine mollusc, Aplysia californica. Following a brief synaptic input, these neuroendocrine cells undergo a 30 min period of firing, known as the afterdischarge, triggering secretion of neuropeptides that initiate egg-laying. I hypothesize that Ca 2+ influx occurs via receptor-mediated activation of a non-selective cation channel and activity-dependent elevation of Ca2+ produces Ca2+ release from intracellular stores. To test this, cultured bag cell neurons were injected with Ca2+ indicator, fura-PE3, and subjected to simultaneous imaging and electrophysiology.; Pharmacological activation of a non-selective cation channel that drives the afterdischarge, produced inward current and, as assessed by Mn 2+-quench of fura, Ca2+ entry. This receptor-operated Ca2+ influx pathway may contribute to plasticity or secretion. Voltage-gated Ca2+ influx was investigated using trains of action potentials delivered at 5 Hz, 10 s (mimicking the synaptic input that initiates the afterdischarge) or 5 Hz, 1 min (mimicking the fast phase of the afterdischarge). While both trains transiently elevated intracellular Ca2+, only the 5 Hz, 1 min stimulus produced a Ca2+ rise that markedly outlasted the initial influx, consistent with Ca2+-induced Ca2+ release (CICR). Thus, robust Ca2+ influx is required to trigger bag cell neuron CICR.; Depletion of the smooth endoplasmic reticulum store, with Ca2+ -ATPase blocker, cyclopiazonic acid, or collapse of the mitochondrial membrane potential, with protonophore, carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone, significantly attenuated CICR. Furthermore, application of tetraphenylphosphonium, a blocker of mitochondrial Ca2+ release, also reduced CICR. Dual depletion of the endoplasmic reticulum and mitochondria did not reduce CICR further than depletion of mitochondria alone. Thus, in departure from the traditional mechanism of CICR, bag cell neuron CICR relies ultimately on mitochondrial Ca2+ release. Finally, intracellular Ca2+ changes during, and after, a stimulus mimicking the full afterdischarge were enhanced by PKC activation. Activity-dependent induction of CICR in bag cell neurons has the potential to influence secretion, membrane currents, or gene expression.
机译：细胞内Ca2 +受细胞外Ca2 +流入和从内部存储释放的影响。根据最初的涌入，可能会产生一系列响应。为了更好地了解围绕Ca2 +处理的过程，我检查了海洋软体动物Aplysia californica的袋状细胞神经元中受体操作或电压门控的Ca 2+流入后的细胞内Ca2 +。在短暂的突触输入后，这些神经内分泌细胞经历了30分钟的放电，称为后放电，触发了引发卵生的神经肽的分泌。我推测，Ca 2+的流入是通过受体介导的非选择性阳离子通道的活化而发生的，并且依赖于活性的Ca2 +升高会导致细胞内存储释放Ca2 +。为了测试这一点，在培养的袋状细胞神经元中注入了Ca2 +指示剂fura-PE3，并同时进行了成像和电生理。非选择性阳离子通道的药理激活，该通道驱动后放电，产生内向电流，并通过呋喃的Mn 2+猝灭评估，Ca2 +进入。该受体操纵的Ca2 +流入途径可能有助于可塑性或分泌。使用在5 Hz，10 s（模仿启动后放电的突触输入）或5 Hz，1 min（模仿后放电的快速阶段）传递的一系列动作电位来研究电压门控的Ca2 +内流。尽管两种训练均会短暂升高细胞内Ca2 +，但只有5 Hz，1分钟的刺激会产生Ca2 +升高，显着超过初始流入量，这与Ca2 +诱导的Ca2 +释放（CICR）一致。因此，需要强大的Ca2 +内流来触发袋细胞神经元CICR。带有Ca2 + -ATPase阻断剂，环吡唑酸的光滑内质网存储的耗尽，或带有质子载体的羰基氰化物4-（三氟甲氧基）苯hydr的线粒体膜电位的破坏，CICR显着减弱。此外，线粒体Ca2 +释放的阻滞剂四苯基phosph的应用也降低了CICR。内质网和线粒体的双重耗竭并没有比单独的线粒体耗竭进一步降低CICR。因此，背离CICR的传统机制，袋细胞神经元CICR最终依赖于线粒体Ca2 +的释放。最后，PKC激活增强了模拟完全放电后刺激过程中和之后的细胞内Ca2 +变化。袋细胞神经元中CICR的活性依赖性诱导具有影响分泌，膜电流或基因表达的潜力。

著录项

  • 作者

    Geiger, Julia Elizabeth.;

  • 作者单位

    Queen's University (Canada).;

  • 授予单位 Queen's University (Canada).;
  • 学科 Biology Cell.; Biology Animal Physiology.
  • 学位 M.Sc.
  • 年度 2008
  • 页码 90 p.
  • 总页数 90
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;生理学;
  • 关键词

  • 入库时间 2022-08-17 11:38:46

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