高压对细胞电压依赖性钙通道的选择调节——一种被提议的 HPNS 部分机制。

Department of Physiology and Neurobiology, Ben Gurion University of the Negev Beer Sheva, Israel.

Department of Physics, Jerusalem College of Technology Jerusalem, Israel.

Front Cell Neurosci. 2014 May 27;8:136. doi: 10.3389/fncel.2014.00136. eCollection 2014.

Professional deep sea divers experience motor and cognitive impairment, known as High Pressure Neurological Syndrome (HPNS), when exposed to pressures of 100 msw (1.1 MPa) and above, considered to be the result of synaptic transmission alteration. Previous studies have indicated modulation of presynaptic Ca(2+) currents at high pressure. We directly measured for the first time pressure effects on the currents of voltage dependent Ca(2+) channels (VDCCs) expressed in Xenopus oocytes. Pressure selectivity augmented the current in CaV1.2 and depressed it in CaV3.2 channels. Pressure application also affected the channels' kinetics, such as ƮRise, ƮDecay. Pressure modulation of VDCCs seems to play an important role in generation of HPNS signs and symptoms.

专业深海潜水员在暴露于 100 米水深（1.1MPa）及以上的压力时会经历运动和认知障碍，称为高压神经综合征（HPNS），这被认为是突触传递改变的结果。先前的研究表明，在高压下，突触前 Ca(2+)电流的调制。我们首次直接测量了压力对在非洲爪蟾卵母细胞中表达的电压依赖性 Ca(2+)通道（VDCCs）电流的影响。压力选择性增强了 CaV1.2 中的电流，而降低了 CaV3.2 通道中的电流。压力施加还影响通道的动力学，例如 ƮRise、ƮDecay。VDCCs 的压力调节似乎在 HPNS 体征和症状的产生中起着重要作用。