Bui B V, Vingrys A J, Kalloniatis Michael
Department of Optometry and Vision Sciences, University of Melbourne, Parkville 3010, Victoria, Australia.
Exp Eye Res. 2003 Aug;77(2):125-36. doi: 10.1016/s0014-4835(03)00132-5.
We wanted to determine the characteristics associated with electrophysiological and neurochemical changes secondary to ischemic insult as well as correlate these electrophysiological and neurochemical changes. A Ganzfeld source was used to elicit electroretinograms in anesthetized adult Sprague-Dawley rats. Following baseline recordings, one eye was removed for control quantitative amino acid immunocytochemistry, and ischemic insult was induced by cervical dislocation. Following the induction of ischemia, a single electroretinogram signal was collected at 1, 2, 4, 6, 8, 16, 32 or 64 min, after which the eye was removed for immunocytochemistry. The post-receptoral b-wave was undetectable after 1 min post-ischemia, whereas phototransduction declined more gradually and persisted for up to 16 min post-mortem. Both phototransduction saturated amplitude and sensitivity decayed with a similar time course (tc=3.06 (2.73, 3.48) versus 3.29 (2.61, 4.62)min). Significant elevation of amino acid neurotransmitter levels was not observed until 6 min post-mortem. Between 8 and 16 min post-ischemia, glutamate and GABA were significantly accumulated in neurons and Müller cells (p<0.05). Beyond 16 min, the neurotransmitter elevation in neurons and Müller cells was relatively attenuated. Aspartate immunoreactivity was significantly elevated at 4 and 6 min post-ischemia in neurons, prior to a change in any other amino acid. Moreover, of the amino acids assessed the post-ischemic change in aspartate immunoreactivity showed the best correlation with phototransduction decay (r2=0.68). Our findings show that complete impairment of phototransduction coincides with the accumulation of amino acid neurotransmitter. The correlation of aspartate immunoreactivity and phototransduction provides evidence of heightened glutamate oxidation during ischemic insult.
我们想要确定继发于缺血性损伤的电生理和神经化学变化的相关特征，并将这些电生理和神经化学变化相互关联起来。使用全视野刺激器在麻醉的成年斯普拉格-道利大鼠中诱发视网膜电图。在进行基线记录后，摘除一只眼睛用于对照定量氨基酸免疫细胞化学分析，通过颈椎脱臼诱导缺血性损伤。在诱导缺血后，于1、2、4、6、8、16、32或64分钟采集单个视网膜电图信号，之后摘除眼睛用于免疫细胞化学分析。缺血后1分钟，感受器后b波无法检测到，而光转导的下降更为缓慢，并在死后持续长达16分钟。光转导饱和振幅和敏感性均以相似的时间进程衰减（时间常数tc = 3.06（2.73，3.48）分钟对3.29（2.61，4.62）分钟）。直到死后6分钟才观察到氨基酸神经递质水平的显著升高。在缺血后8至16分钟之间，谷氨酸和γ-氨基丁酸在神经元和米勒细胞中显著积累（p<0.05）。超过16分钟后，神经元和米勒细胞中神经递质的升高相对减弱。在任何其他氨基酸发生变化之前，神经元中缺血后4至6分钟天冬氨酸免疫反应性显著升高。此外，在所评估的氨基酸中，缺血后天冬氨酸免疫反应性的变化与光转导衰减的相关性最佳（r2 = 0.68）。我们的研究结果表明，光转导的完全受损与氨基酸神经递质的积累同时发生。天冬氨酸免疫反应性与光转导的相关性为缺血性损伤期间谷氨酸氧化增强提供了证据。
