Miyashita K, Abe H, Nakajima T, Ishikawa A, Nishiura-Suzuki M, Naritomi H, Tanaka R, Sawada T
Department of Medicine, National Cardiovascular Centre, Osaka, Japan.
Neuroreport. 1994 Apr 14;5(8):945-8. doi: 10.1097/00001756-199404000-00023.
In a modified version of the unilateral middle cerebral artery occlusion (MCAO) model in gerbils, both sides of hippocampus are spared from direct ischaemic insult. Using this newly employed left MCAO model in gerbils, we investigated the concentrations of extracellular amino acids in the left hippocampus by microdialysis and histological changes in both sides of hippocampus one month after ischaemia. The concentrations of glutamate and aspartate were significantly increased by more than 3.5 times basal levels after MCAO. Glutamate maintained this peak level for 40 to 120 min after the onset of ischaemia. However, hippocampal neurones were well preserved one month after MCAO. While the exact mechanism of the survival of hippocampal neurones remains to be elucidated, we suggest it may be crucial that the hippocampus be protected from ischaemic insult.
在沙土鼠单侧大脑中动脉闭塞（MCAO）模型的改良版本中，双侧海马均未受到直接缺血性损伤。利用这种新采用的沙土鼠左侧MCAO模型，我们通过微透析研究了缺血后1个月左侧海马细胞外氨基酸的浓度以及双侧海马的组织学变化。MCAO后谷氨酸和天冬氨酸的浓度显著增加，超过基础水平的3.5倍。缺血开始后，谷氨酸在40至120分钟内维持这一峰值水平。然而，MCAO后1个月海马神经元保存良好。虽然海马神经元存活的确切机制仍有待阐明，但我们认为海马免受缺血性损伤可能至关重要。
