[Ca2+]和[H+]对体外缺氧损伤大鼠脑突触体功能恢复的影响。
The effect of [Ca2+] and [H+] on the functional recovery of rat brain synaptosomes from anoxic insult in vitro.
作者信息
Harvey S A, Booth R F, Clark J B
出版信息
Biochem J. 1983 May 15;212(2):289-95. doi: 10.1042/bj2120289.
The energy status (as measured by the ATP/ADP ratio), oxidative metabolism (14CO2 output) and neurotransmitter synthesis ( [14C]acetylcholine production) by rat brain synaptosomes utilizing [U-14C]glucose has been studied. The ability of anoxia in vitro to permanently alter these parameters was investigated with reference to external [Ca2+] and [H+]. It has previously been shown that anoxic damage to synaptosomal preparations is only apparent when their metabolism is stimulated by veratridine [Harvey, Booth & Clark (1982) Biochem. J. 206, 433-439]. It is concluded that low [Ca2+] ameliorates, and high [H+] exacerbates, the damage sustained by veratridine-stimulated anoxic synaptosomes. The combined effects of low pH, anoxia and veratridine stimulation on synaptosomal metabolism most closely approximated to the irreversible damage to brain metabolism observed during acute hypoxia in vivo [Booth, Harvey & Clark (1983) J. Neurochem. 40, 106-110]. Suitably treated synaptosomal preparations may therefore be usefully employed as models to study impaired neurotransmitter synthesis in vivo.
已对利用[U-¹⁴C]葡萄糖的大鼠脑突触体的能量状态（通过ATP/ADP比率测量）、氧化代谢（¹⁴CO₂输出）和神经递质合成（[¹⁴C]乙酰胆碱产生）进行了研究。参照细胞外[Ca²⁺]和[H⁺]，研究了体外缺氧对这些参数的永久性改变能力。先前已经表明，只有当藜芦碱刺激突触体制剂的代谢时，缺氧对突触体制剂的损伤才会显现出来[哈维、布斯和克拉克（1982年）《生物化学杂志》206, 433 - 439]。得出的结论是，低[Ca²⁺]可改善，高[H⁺]会加剧藜芦碱刺激的缺氧突触体所遭受的损伤。低pH、缺氧和藜芦碱刺激对突触体代谢的综合影响最接近体内急性缺氧期间观察到的对脑代谢的不可逆损伤[布斯、哈维和平克拉克（1983年）《神经化学杂志》40, 106 - 110]。因此，经过适当处理的突触体制剂可有效地用作研究体内神经递质合成受损的模型。
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