Different mechanisms of secondary neuronal damage in thalamic nuclei after focal cerebral ischemia in rats
Different mechanisms of secondary neuronal damage in thalamic nuclei after focal cerebral ischemia in rats
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DOI：
10.1161/01.str.0000039406.64644.cb
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发表时间：
2002-12-01
期刊：
影响因子：
8.3
通讯作者：
Block, F
中科院分区：
文献类型：
--
作者：
Dihné, M;Grommes, C;Block, F
背景和目的：局灶性脑缺血后，根据其局部和程度的不同，继发性神经元损伤可能发生在远离初始病变的地方。本研究采用不同的缺血模型，观察丘脑腹后核（VPN）和网状核（RTN）继发性损伤的差异。方法：短暂性大脑中动脉闭塞（MCAO）导致皮质梗死，包括基底神经节的部分，如苍白球，以及广泛的水肿。光血栓性缺血产生纯粹的皮质梗死，保留基底节区，仅伴有轻微水肿。缺血14天后，在同侧RTN和VPN内量化神经元变性。应用免疫组织化学方法研究神经胶质反应。结果：mcao导致同侧VPN和RTN神经元细胞损失延迟。24小时后，两个核开始出现神经胶质活化。光血栓性缺血仅在VPN内导致延迟的神经元细胞损失。即使在光血栓性缺血2周后，也只能在VPN内观察到胶质细胞的激活。结论：光血栓性缺血后的单纯皮质梗死，无严重水肿，对基底节区苍白球无影响，仅导致继发性VPN损伤，可能是由于逆行变性。MCAO导致皮层和苍白球梗死，引起广泛水肿，导致VPN和RTN继发性损伤。因此，额外的RTN损伤可能是由于从苍白球到RTN的保护性gaba能输入的丧失或由于广泛的水肿。逆行性退行性变是不可能的，因为与VPN相反，RTN对皮层没有传出。
Background and Purpose-After focal cerebral ischemia, depending on its localization and extent, secondary neuronal damage may occur that is remote from the initial lesion. In this study differences in secondary damage of the ventroposterior thalamic nucleus (VPN) and the reticular thalamic nucleus (RTN) were investigated with the use of different ischemia models.Methods-Transient middle cerebral artery occlusion (MCAO) leads to cortical infarction, including parts of the basal ganglia such as the globus pallidus, and to widespread edema. Photothrombotic ischemia generates pure cortical infarcts sparing the basal ganglia and with only minor edema. Neuronal degeneration was quantified within the ipsilateral RTN and VPN 14 days after ischemia. Glial reactions were studied with the use of immunohistochemistry.Results-MCAO resulted in delayed neuronal cell loss of the ipsilateral VPN and RTN. Glial activation occurred in both nuclei beginning after 24 hours. Photothrombotic ischemia resulted in delayed neuronal cell loss only within the VPN. Even 2 weeks after photothrombotic ischemia, glial activation could only be seen within the VPN.Conclusions-Pure cortical infarcts after photothrombotic ischemia, without major edema and without effects on the globus pallidus of the basal ganglia, only lead to secondary VPN damage that is possibly due to retrograde degeneration. MCAO, which results in infarction of cortex and globus pallidus and which causes widespread edema, leads to secondary damage in the VPN and RTN. Thus, additional RTN damage may be due to loss of protective GABAergic input from the globus pallidus to the RTN or due to the extensive edema. Retrograde degeneration is not possible because the RTN, in contrast to the VPN, has no efferents to the cortex.