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Actions of NCX, PMCA and SERCA on Short-Term Facilitation and Maintenance of Transmission in Nerve Terminals

机译:NCX,PMCA和SERCA在短期促进和维护神经终端传输中的作用

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Residual Ca2+ can accumulate in the nerve terminal during repetitive stimulation; thus, the basis for short-termfacilitation (STF). The plasmalemmal Na+/Ca2+ exchanger [NCX], the Ca2+-ATPase (PMCA) and thesarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) on the endoplasmic reticulum are three important Ca2+regulatory processes in controlling [Ca2+]i. The role of these [Ca2+]i regulators in the development and maintenance ofSTF was addressed at the neuromuscular junction. When the NCX is compromised by reduced [Na+]o, the EPSPamplitudes decrease, but with KB-R7943 (a reverse blocker of NCX) the amplitude increases. Compromising the PMCAwith pH 8.8 produces an increase in EPSP amplitudes, but treatments with carboxyeosin (a blocker of PMCA) producedmixed results. Blocking the SERCA increases EPSP amplitudes. Facilitation was only slighted altered in some conditionswith these manipulations. The results support the view that release is not saturated during a plateau phase of STF since theterminal is able to reach a new plateau with higher stimulation frequency or an altered [Ca2+]i. Multiple approaches incompromising the NCX and PMCA are presented. These findings are significant because there is a rapid alteration intransmission when compromising Ca2+ extrusion mechanisms during STF.
机译:在重复刺激过程中,残留的Ca2 +会积聚在神经末梢;因此,这是短期便利化(STF)的基础。内质网上的质膜Na + / Ca2 +交换子[NCX],Ca2 + -ATPase(PMCA)和质膜/内质网Ca2 + -ATPase(SERCA)是控制[Ca2 +] i的三个重要的Ca2 +调节过程。这些[Ca2 +] i调节剂在STF的形成和维持中的作用在神经肌肉接头处得到解决。当NCX因[Na +] o降低而受损时,EPSPamplitudes减小,但是使用KB-R7943(NCX的反向阻止器)时,振幅增大。用pH 8.8破坏PMCA会增加EPSP幅度,但是用羧曙红(PMCA的阻滞剂)处理会产生混合结果。阻塞SERCA会增加EPSP幅度。通过这些操作,便利化仅在某些情况下有所改变。结果支持这样的观点,即在STF的平台期释放不会饱和,因为终端能够以更高的刺激频率或[Ca2 +] i改变达到新的平台。提出了多种折衷NCX和PMCA的方法。这些发现意义重大,因为在STF期间损​​害Ca2 +挤出机制时,会迅速改变透射率。

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