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脑缺血再灌流导致海马CA1锥体细胞溃变而CA3神经元依然存活，这种选择性损伤的机制尚不清楚。两区间抑制性神经成分的差异可能是原因之一。本文用免疫细胞化学方法研究了上述假设的形态基础。在光镜下，CA1和CA3区每个锥体细胞环胞体的GABA阳性终末数分别是7.02±2.06和10.10±3.02（P＜0.001），每单位膜长度上的阳性终末数CA1也较CA3有意义的少。电镜下，GABA能终末与锥体细胞胞体形成对称性突触，CA1和CA3区锥体细胞的环胞体GABA阳性突触数分别是6.36±1.59和10.68±2.28（P＜0.01）。胞体膜被GABA能突触所覆盖的面分比也有显著差异（CA3=13.9±3.36％，CA1=10.9±5.06％，P＜0.001）。结果表明CA1神经元胞体较CA3神经元受到较少的GABA能支配。此点可能在脑缺血后CA1细胞较CA3细胞易损害机制中发挥作用。
Cerebral ischemia-reperfusion leads to the degeneration of pyramidal cells in hippocampal CA1 neurons and the survival of CA3 neurons. The mechanism of this selective injury is not clear yet. The difference between the two inhibitory neurological components may be one of the reasons. In this paper, immunocytochemistry was used to study the morphological basis of the above hypotheses. Under light microscopy, the number of GABA-positive terminals per circular body of pyramidal cells in CA1 and CA3 were 7.02 ± 2.06 and 10.10 ± 3.02, respectively (P <0.001), and the number of positive terminal CA1 per unit length CA3 less meaningful. Under electron microscope, GABA could form symmetrical synapses with pyramidal cell bodies and the numbers of GABA-positive synapses in CA1 and CA3 pyramidal cells were 6.36 ± 1.59 and 10.68 ± 2.28, respectively (P <0.01). There was also a significant difference in surface area ratio covered by GABAergic synapses (CA3 = 13.9 ± 3.36%, CA1 = 10.9 ± 5.06%, P <0.001). The results show that CA1 neuronal somatic cells are less GABA-dominated than CA3 neurons. This may be in the CA1 cells after cerebral ischemia than CA3 cells play a role in the mechanism of vulnerability.