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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Enhancement of AMPA-mediated current after traumatic injury in cortical neurons.
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Enhancement of AMPA-mediated current after traumatic injury in cortical neurons.

机译：皮质神经元外伤后AMPA介导的电流增强。

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摘要

Overactivation of ionotropic glutamate receptors has been implicated in the pathophysiology of traumatic brain injury. Using an in vitro cell injury model, we examined the effects of stretch-induced traumatic injury on the AMPA subtype of ionotropic glutamate receptors in cultured neonatal cortical neurons. Recordings made using the whole-cell patch-clamp technique revealed that a subpopulation of injured neurons exhibited an increased current in response to AMPA. The current-voltage relationship of these injured neurons showed an increased slope conductance but no change in reversal potential compared with uninjured neurons. Additionally, the EC(50) values of uninjured and injured neurons were nearly identical. Thus, current potentiation was not caused by changes in the voltage-dependence, ion selectivity, or apparent agonist affinity of the AMPA channel. AMPA-elicited current could also be fully inhibited by the application of selective AMPA receptor antagonists, thereby excluding the possibility that current potentiation in injured neurons was caused by the activation of other, nondesensitizing receptors. The difference in current densities between control and injured neurons was abolished when AMPA receptor desensitization was inhibited by the coapplication of AMPA and cyclothiazide or by the use of kainate as an agonist, suggesting that mechanical injury alters AMPA receptor desensitization. Reduction of AMPA receptor desensitization after brain injury would be expected to further exacerbate the effects of increased postinjury extracellular glutamate and contribute to trauma-related cell loss and dysfunctional synaptic information processing.
机译：离子型谷氨酸受体的过度活化与创伤性脑损伤的病理生理学有关。使用体外细胞损伤模型，我们检查了拉伸诱导的创伤性损伤对培养的新生儿皮质神经元中离子型谷氨酸受体AMPA亚型的影响。使用全细胞膜片钳技术进行的记录显示，受损的神经元亚群对AMPA的反应电流增加。与未受伤的神经元相比，这些受伤的神经元的电流-电压关系显示出增加的斜率电导，但是反转电位没有变化。此外，未受伤和受伤的神经元的EC（50）值几乎相同。因此，电流增强不是由AMPA通道的电压依赖性，离子选择性或表观激动剂亲和力的变化引起的。还可通过使用选择性AMPA受体拮抗剂来完全抑制AMPA引起的电流，从而排除了受损神经元中电流增强是由其他非脱敏受体激活引起的可能性。当同时使用AMPA和环噻嗪或使用海藻酸盐作为激动剂抑制AMPA受体脱敏时，​​对照神经元和受损神经元之间电流密度的差异将被消除，这表明机械损伤会改变AMPA受体脱敏。预期脑损伤后AMPA受体脱敏的减少将进一步加重损伤后细胞外谷氨酸的增加，并导致创伤相关的细胞丢失和功能异常的突触信息处理。

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