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首页> 外文期刊>Undersea and Hyperbaric Medicine: Journal of the Undersea and Hyperbaric Medical Society >Cellular and neurophysiological effects of high ambient pressure.
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Cellular and neurophysiological effects of high ambient pressure.

机译：细胞和神经生理学的影响高环境的压力。

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The observed cellular effects of pressure are entirely compatible with the acute manifestations of CNS hyperexcitability. Inhibition of the glycine receptor will reduce post-synaptic inhibition, leading to increased excitability (cf 'Startle Disease', an hereditary disease with increased excitability arising from a genetic modification to the glycine receptor (Becker et al., 2002)). Since glycine-mediated neurotransmission is particularly associated with motor reflex circuits (Lynch, 2004) it is not surprising that many of the acute manifestations of pressure involve motor dysfunction. Potentiation by pressure of the NR1-NR2C subtype of the NMDA-sensitive glutamate receptor will lead to increased excitability within the cerebellum (where this receptor sub-type is most highly expressed (Monyer et al., 1994)). Although the cerebellum receives input from many parts of the nervous system, it projects primarily to the motor and frontal lobe cognitive areas. Thus dysfunction of the glutamate-mediated excitatory neurotransmission in this area is most likely to result in locomotor and cognitive symptoms, characteristic of acute pressure effects. Finally, the effects observed on AC/cAMP intracellular signalling, probably mediated via dopamine receptors, is also likely to produce motor dysfunction (cf Parkinson's disease). The observed cellular effects also suggest potential mechanisms that could result in long-term CNS dysfunction. Potentiation of glutamate neurotransmission is likely to lead to excessive calcium entry into those neurons. This may trigger excitotoxicity via a signal cascade in which neuronal NO synthase is activated producing the toxic free radical peroxynitrite and activation of the proapoptotic protein poly(ADP-ribose) polymerase (Aarts & Tymianski, 2005). An additional mechanism, also initially triggered by a rise in intracellular calcium through NR1-NR2C receptors, involves activation of a member of the Transient Receptor Potential (TRP) channel superfamily, the TRPM-7 channel. Activation of these channels will cause a further rise in intracellular calcium, creating a positive feedback and generating more neuronal death through the toxic signal cascade (Aarts & Tymianski, 2005). Neuronal cell death within the cerebellum might be expected to give rise to delayed motor and cognitive dysfunction the magnitude of which would tend to be related to the extent of hyperbaric exposure. There is at present no evidence that these excitotoxic mechanisms are triggered by exposure to pressure but future experimental work should investigate the extent to which pressure might activate them.
机译：观察到的细胞压力的影响急性症状完全兼容中枢神经系统兴奋过度。甘氨酸受体将减少突触后抑制,导致兴奋性增加(cf惊吓的疾病,一种遗传性疾病基因引起的兴奋性增加修改甘氨酸受体(贝克等, 2002))。神经传递尤其相关电动机反射回路(林奇,2004)奇怪的许多急性症状的压力包括运动功能障碍。增强作用NR1-NR2C亚型的压力NMDA-sensitive谷氨酸受体的意志导致内兴奋性增加小脑(这个受体亚型高表达(许多et al ., 1994))。从许多地方小脑接收输入神经系统,主要的it项目电机和额叶认知领域。glutamate-mediated兴奋性的障碍神经传递在这个领域是最有可能的导致运动和认知症状,急性压力影响的特征。最后,观察对AC /阵营的影响胞内信号,可能通过介导的多巴胺受体,也可能产生运动功能障碍(cf帕金森症)。观察细胞也表明潜在的影响机制,可能导致长期的中枢神经系统功能障碍。神经传递可能导致过度钙进入这些神经元。通过信号级联触发器会引起神经元没有合酶被激活产生有毒的自由基和过氧亚硝基的激活proapoptotic蛋白质保利(ADP-ribose)聚合酶(艾亚茨& Tymianski2005)。引发了细胞内钙通过NR1-NR2C受体,包括激活瞬时受体电位的一员(TRP)通道总科,TRPM-7通道。激活这些渠道将进一步导致增加细胞内钙、创建一个积极的反馈和生成更多的神经元通过有毒信号级联(艾亚茨和死亡Tymianski, 2005)。小脑可能产生延迟运动和认知功能障碍的大小往往是相关的高压暴露的程度。目前没有证据表明这些excitotoxic机制引发的接触压力但今后的实验工作应该调查压力可能会激活他们的程度。

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