引用

神经元损伤是新生儿缺氧缺血性脑损伤的一个重要特征。然而，人们对神经元损失的机制(如脑干)知之甚少。一种可能性是，大脑皮层和脑干之间的神经连接被破坏，可能会危及脑干中神经元细胞体的存活。我们研究了HI后脑干中投射到皮层的血清素能神经元是否丢失。我们还测试了神经炎症是否在干扰脑干投影中起作用。出生后第3天(P3)大鼠行单侧颈动脉结扎，缺氧(6%氧30min)。逆行示踪剂choleratoxin b在P38运动皮层沉积。在P45上，我们发现在P3 HI后，背侧核、腹侧核、束间核、尾侧核和腹侧核的逆行标记神经元丢失。所有在raph核中逆行标记的神经元都是血清素能。逆行标记的神经元数量在丘脑腹内侧和杏仁核基底外侧也减少了。 Minocycline treatment (45 mg/kg 2h post-HI, 22.5 mg/kg daily P4-P9) attenuated losses of retrogradely labelled neurons in the dorsal raph ventrolateral, interfascicular and ventral raph nuclei, and the ventromedial thalamus. These results indicate that raph neurons projecting to the cortex constitute a population of serotonergic neurons that are lost after P3 HI. Furthermore, neuroinflammation has a role in the disruption of raph and thalamic neural projections. Future studies investigating the cellular mechanisms of axonal degeneration may reveal new targets for interventions to prevent neuronal losses after neonatal HI.