Johansen F F, Zimmer J, Diemer N H
Acta Neuropathol. 1987;73(2):110-4. doi: 10.1007/BF00693775.
Somatostatin (SS)- and cholecystokinin (CCK)-immunopositive cell somata in the rat hippocampus were quantitated at day 1, 2, 3 and 4 after cerebral ischemia. A significant (P less than 0.01) 60%-80% loss of hilar and CA-3c SS neurons took place. No CCK neurons were lost. Damage to SS neurons was significant on the second postischemic day and preceded the delayed loss of CA-1 neurons. We speculate that loss of SS neurons, which presumably innervate the inhibitory GABAergic (gamma-aminobutyric acid) interneurons, may induce hyperactivity stimulating the Ca-1 neurons to death.
在大脑缺血后的第1、2、3和4天,对大鼠海马中生长抑素(SS)和胆囊收缩素(CCK)免疫阳性细胞体进行了定量分析。海马门区和CA-3c区的SS神经元显著(P<0.01)损失了60%-80%。CCK神经元没有损失。缺血后第二天,SS神经元的损伤很明显,且早于CA-1神经元的延迟性损失。我们推测,SS神经元的损失可能会诱发过度活动,刺激Ca-1神经元死亡,据推测,SS神经元支配抑制性GABA能(γ-氨基丁酸)中间神经元。