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首页> 外文期刊>The European Journal of Neuroscience >Changes in neuronal response to ischemia in retinas with genetic alterations of somatostatin receptor expression.
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Changes in neuronal response to ischemia in retinas with genetic alterations of somatostatin receptor expression.

机译：视网膜生长激素受体表达的遗传改变对视网膜缺血神经元反应的变化。

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摘要

Ischemia is a primary cause of neuronal death in retinal diseases. The repertoire of expressed transmitter receptors would determine the neurons' responses to ischemic damage, and peptidergic receptors may be involved. With a new in vitro model of the ischemic mouse retina, we investigated whether an altered expression of somatostatin receptors could modulate retinal responses to ischemia. We used retinas of somatostatin receptor 1 (sst(1)) knock out (KO) mice, where sst(2) are over-expressed and over-functional, and of sst(2) KO mice. TUNEL analysis of ischemic retinas showed a marked reduction of cell death in sst(1) KO retinas, while there were no differences between wild-type (WT) and sst(2) KO retinas. In addition, caspase-3 mRNA expression was also reduced in sst(1) KO as compared to WT retinas. An immunohistochemical analysis demonstrated that different cell populations responded differently to the ischemic insult, and that the persistence of some immunohistochemical markers was greater in sst(1) KO than in WT or in sst(2) KO retinas. In particular, rod bipolar cell survival was markedly improved in sst(1) KO retinas, while it was dramatically decreased in sst(2) KO retinas. Furthermore, consistent with a role of glutamate excitotoxicity in ischemia-induced neuronal death, retinal glutamate release was observed to increase under ischemic conditions, but this increase was significantly reduced in sst(1) KO retinas. These observations demonstrate that an increased presence of functional sst(2) protects against retinal ischemia, thus implementing the background for the use of sst(2) analogs in therapies of retinal diseases such as glaucoma or diabetic retinopathy.
机译：缺血是视网膜疾病中神经元死亡的主要原因。表达的递质受体的库将决定神经元对缺血性损伤的反应，并且可能牵涉肽能受体。使用缺血小鼠视网膜的新的体外模型，我们调查了生长抑素受体表达的改变是否可以调节视网膜对局部缺血的反应。我们使用了生长抑素受体1（sst（1））敲除（KO）小鼠的视网膜，其中sst（2）过表达和功能过度，并且使用了sst（2）KO小鼠的视网膜。缺血性视网膜的TUNEL分析显示sst（1）KO视网膜细胞死亡明显减少，而野生型（WT）和sst（2）KO视网膜之间没有差异。此外，与WT视网膜相比，sst（1）KO中的caspase-3 mRNA表达也降低了。免疫组织化学分析表明，不同的细胞群体对缺血损伤的反应不同，并且某些免疫组织化学标记物在sst（1）KO中的持久性大于在WT或sst（2）KO视网膜中。特别是，杆状双极细胞存活率在sst（1）KO视网膜中显着提高，而在sst（2）KO视网膜中则显着降低。此外，与谷氨酸兴奋性毒性在局部缺血引起的神经元死亡中的作用一致，在缺血条件下视网膜谷氨酸的释放增加，但在sst（1）KO视网膜中这种减少显着减少。这些观察结果表明，功能性sst（2）的存在增加可防止视网膜缺血，从而为在诸如青光眼或糖尿病性视网膜病等视网膜疾病的治疗中使用sst（2）类似物提供了背景。

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