MICROSENSOR TECHNOLOGY TO MEASURE FAST EXTRACELLULAR EVENTS

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 钙离子诱导的心肌细胞钙释放（CICR）在心肌细胞的二进空间内表现出梯度性和高增益。在心肌细胞中这种Ca 2+信号传导的中断可以激活病理性肥大，从而引发心脏病。虽然细胞水平的CICR已被广泛建模，但L型Ca 2+通道的单次开放与心肌细胞中Ca 2+的量子细胞内释放（火花）之间的相关性仍未得到证实。 离子通道的研究从膜片钳技术中受益匪浅，它允许以无与伦比的分辨率测量单通道电流。即便如此，膜片钳对细胞的侵入性相对较强，破坏了细胞内信号转导，特别是局部CICR途径。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Calcium (Ca2+)-induced calcium-release (CICR) within the dyadic space of cardiac myocytes displays gradedness and high gain. Disruption of this Ca2+ signalling in the myocyte can activate pathological hypertrophy and thus heart disease. While CICR at the cellular level has been extensively modeled, the correlation between single openings of the L-type Ca2+ channel and the quantal intracellular release of Ca2+ (sparks) in cardiac myocytes remains unsubstantiated. Studies of ion channels have benefited greatly from patch-clamping, allowing single channel currents to be measured with unparalleled resolution. Even so, patch clamping is relatively invasive to the cell, disrupting intracellular signal transduction, particularly local CICR pathways.