Yasui M, Kawasaki K
Division of Pharmacology, Shionogi & Co., Ltd., Osaka, Japan.
Neurosci Lett. 1995 May 19;191(1-2):99-102. doi: 10.1016/0304-3940(95)11570-0.
We examined the effect of cholecystokinin octapeptide sulfated type (CCK-8S) on dysfunction of CA1 pyramidal neurons induced by in vitro ischemic insult in hippocampal slices of stroke-prone spontaneously hypertensive rats (SHRSP). CCK-8S shortened the time required for partial recovery from block of a population spike produced by ischemia. Furthermore, CCK-8S reduced ischemic insult-induced accumulation of K+ in extracellular space. Suppression of the K+ conductance by the CCKB receptor activation is suggested to contribute to neuroprotection by CCK-8S.
我们研究了硫酸化八肽胆囊收缩素（CCK-8S）对易卒中型自发性高血压大鼠（SHRSP）海马切片体外缺血损伤诱导的CA1锥体神经元功能障碍的影响。CCK-8S缩短了缺血引起的群体峰电位阻断部分恢复所需的时间。此外，CCK-8S减少了缺血损伤诱导的细胞外空间K+的积累。提示CCKB受体激活对K+电导的抑制作用有助于CCK-8S的神经保护作用。
