Korematsu K, Goto S, Nagahiro S, Ushio Y
Department of Neurosurgery, Kumamoto University Medical School, Japan.
Brain Res. 1993 Jul 9;616(1-2):320-4. doi: 10.1016/0006-8993(93)90225-c.
We assessed the chronological change of the expression of synaptophysin, an integral glycoprotein on the presynaptic vesicles, after a transient cerebral ischemic insult in the rat. The ischemic lesion was consistently localized in the dorsolateral part of the striatum, which was clearly visualized by a depletion of calcineurin immunostaining or increases of immunoreactivities for glial fibrillary acidic protein and tyrosine hydroxylase. Immunoreactivity for synaptophysin was transiently increased in the ischemic lesions from 3 to 7 days after cerebral ischemia. Thereafter, synaptophysin immunostaining in the damaged areas gradually decreased and finally almost disappeared one month after surgery. Because synaptophysin is located in the presynaptic vesicle, and thought to be involved in presynaptic functions such as vesicle-membrane fusion and release of neurotransmitters, present findings suggest that loss of the postsynaptic site after ischemic insult induces a transient increase of the presynaptic functions, followed by a decrease of functional presynaptic activity or trans-synaptic retrograde degeneration of axon terminals.
我们评估了大鼠短暂性脑缺血损伤后，突触囊泡膜固有糖蛋白突触素表达的时间变化。缺血性病变始终位于纹状体的背外侧部分，通过钙调神经磷酸酶免疫染色缺失或胶质纤维酸性蛋白和酪氨酸羟化酶免疫反应性增加可清晰观察到。脑缺血后3至7天，缺血性病变中突触素的免疫反应性短暂增加。此后，受损区域的突触素免疫染色逐渐减少，术后一个月最终几乎消失。由于突触素位于突触前囊泡中，且被认为参与突触前功能，如囊泡-膜融合和神经递质释放，目前的研究结果表明，缺血性损伤后突触后位点的丧失会导致突触前功能短暂增加，随后是功能性突触前活动的减少或轴突终末的跨突触逆行变性。
