Lei Zhigang, Ruan Yiwen, Yang Angela N, Xu Zao C
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Neurosci Lett. 2006 Oct 30;407(3):224-9. doi: 10.1016/j.neulet.2006.06.019. Epub 2006 Sep 18.
Dendrites and spines undergo dynamic changes in physiological and pathological conditions. Dendritic outgrowth has been observed in surviving neurons months after ischemia, which is associated with the functional compensation. It remains unclear how dendrites in surviving neurons are altered shortly after ischemia, which might reveal the mechanisms underlying neuronal survival. Using primary cortical cultures, we monitored the dendritic changes in individual neurons after oxygen-glucose deprivation (OGD). Two to four hours of OGD induced approximately 30-50% cell death in 24 h. However, the total dendritic length in surviving neurons was significantly increased after OGD with a peak at 6 h after re-oxygenation. The increase of dendritic length after OGD was mainly due to the sprouting rather than the extension of the dendrites. The dendritic outgrowth after 2 h of OGD was greater than that after 4 h of OGD. Application of NMDA receptor blocker MK-801 abolished OGD-induced dendritic outgrowth, whereas application of AMPA receptor antagonist CNQX had no significant effects. These results demonstrate a NMDA receptor-dependent dendritic plasticity shortly after OGD, which provides insights into the early response of surviving neurons after ischemia.
树突和树突棘在生理和病理条件下会发生动态变化。在缺血数月后的存活神经元中观察到树突生长，这与功能代偿有关。目前尚不清楚缺血后不久存活神经元中的树突是如何改变的，这可能揭示神经元存活的潜在机制。我们使用原代皮质培养物，监测了氧糖剥夺（OGD）后单个神经元的树突变化。两到四小时的OGD在24小时内诱导约30 - 50%的细胞死亡。然而，OGD后存活神经元的总树突长度显著增加，在复氧后6小时达到峰值。OGD后树突长度的增加主要是由于树突的萌发而非延伸。2小时OGD后的树突生长大于4小时OGD后的树突生长。应用NMDA受体阻滞剂MK - 801可消除OGD诱导的树突生长，而应用AMPA受体拮抗剂CNQX则无显著影响。这些结果表明OGD后不久存在NMDA受体依赖性树突可塑性，这为缺血后存活神经元的早期反应提供了见解。
