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首页> 外文期刊>Journal of Cellular Physiology >Ionic channels and neuropathic pain: physiopathology and applications.
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Ionic channels and neuropathic pain: physiopathology and applications.

机译：离子通道和神经性疼痛:生理病理学和应用程序。

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Neuropathic pain is defined by the International Association for Pain research as a pain associated to a primary lesion or a dysfunction of the central or peripheral system. Over the past few years the causes of the neuropathic pain were not known and there were not good treatments for it, now we have a better knowledge of the physiopathological aspects and there is a wider diffusion of the research for target aimed therapies. The physiologic genesis of nervous messages occurs exclusively in skin sensorial endings or in nerve tissues as a consequence of an adequate sensorial stimulus and depends on the quick variations of the electric potential difference at the endings of ionic membranes. These variations of even 500 V a second are possible because of the presence of ionic channels. In neuropathic pain impulses can be originated even from ectopic sites. Ectopic discharges originated in a peripheral neuropathic system have an important role in the early stage of neuropathic pain development in two different ways. First they give an excess of spontaneous and evoked electric impulses to the central nervous system, causing a primitive neuropathic pain signal; then the ectopic activity develops and maintains the central sensitisation process. All this amplifies the afferent signals deriving from residual efferents that go on innerving cutaneous areas damaged and partly disnerved, causing tactile allodynie. Sodium channels are the greatest responsible for electrogenesis, that is the basis of the action potential generation and its propagation. Action potential begins after a depolarization such that it could cause a membrane transitory modification, turning prevalently permeable to Na+ more than to K+ as during a release phase. Neuropathy generates a local accumulation of sodium channels, with a consequent increase of density. This remodel seems to be the basis of neuro hyperexecitably. Calcium channels have also an important role in cell working. Intracellular calcium increase contributes to depolarizationprocesses, through kinase and determines the phosphorylation of membrane proteins that can make powerful the efficacy of the channels themselves. In the future new diagnostic opportunities of physiopathologist mechanism leading to neuropathic pain will allow treatments aimed at specific molecular changes of ionic channels.
机译：神经性疼痛的定义是由国际疼痛研究协会是一个痛苦主要病变或功能障碍有关中央或外围系统。过去几年神经性疼痛的原因不知道,没有好的治疗方法吗,现在我们有一个更好的了解有一个更广泛的physiopathological方面扩散的研究目标的目的疗法。消息只发生在皮肤感觉的结局或神经组织的结果一个足够的感觉的刺激和依赖快速变化的电势不同结局的离子膜。这些变化甚至每秒500 V可能由于离子的存在频道。甚至是来自异位网站。排放起源于周围神经性系统在早期阶段一个重要的角色在两个不同的神经性疼痛的发展的方式。和中央诱发电冲动神经系统,造成原始神经性疼痛信号;和维护中枢敏化作用的过程。这一切都放大了传入信号推导从残余继续刺激神经的传出皮肤受损,部分disnerved地区,导致触觉allodynie。最大的负责产电,动作电位产生的基础吗和它的传播。后去极化,使其可能导致膜暂时的修改,把普遍地渗透Na + K +多在释放阶段。当地积累的钠离子通道,密度随之增加。似乎神经hyperexecitably的基础。钙通道也非常重要的作用电池工作。有助于depolarizationprocesses通过激酶的磷酸化,并确定膜蛋白可以使强大的通道本身的效果。未来的新的诊断的机会physiopathologist机制导致神经性疼痛将允许针对治疗特定的分子离子通道的变化。

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