Saijoh K, Fujiwara H, Tanaka C
Jpn J Pharmacol. 1985 Dec;39(4):529-39. doi: 10.1254/jjp.39.529.
We studied the influence of hypoxia on the release of [3H]dopamine ([3H]DA) and [3H]acetylcholine ([3H]ACh), uptake of [3H]DA and [3H]choline and Ca2+-influx in guinea pig striatal slices. Tetrodotoxin (TTX)-sensitive and Ca2+-dependent electrically evoked release of [3H]DA was not affected by hypoxia, while spontaneous release of [3H]DA was rapidly increased. On the other hand, by hypoxia, the evoked [3H]ACh release gradually decreased and was diminished to about 45% 40 min later. Hypoxia suppressed the Vmax of [3H]DA uptake to one third and that of [3H]choline to half of the control values, but with no change in either of the Km values. Hypoxia reduced both the acetylation and the uptake of [3H]choline in slices preliminarily incubated with 3 mM or 25 mM K+ medium. Stimulation-induced Ca2+-influx was slightly suppressed and was 78.1% of the control values even after 40 min exposure to hypoxia. The Ca2+-dependent neurotransmitter release process itself appears to be well preserved against hypoxia as compared with the uptake process. Our findings imply that hypoxia could result in differential alterations of neural activity depending on the specific sensitivity of the presynaptic process of neurotransmission.
我们研究了缺氧对豚鼠纹状体切片中[3H]多巴胺（[3H]DA）和[3H]乙酰胆碱（[3H]ACh）释放、[3H]DA和[3H]胆碱摄取以及Ca2+内流的影响。河豚毒素（TTX）敏感且依赖Ca2+的电诱发[3H]DA释放不受缺氧影响，而[3H]DA的自发释放迅速增加。另一方面，缺氧使诱发的[3H]ACh释放逐渐减少，40分钟后降至约45%。缺氧将[3H]DA摄取的Vmax抑制至对照值的三分之一，将[3H]胆碱摄取的Vmax抑制至对照值的一半，但两个Km值均无变化。缺氧降低了预先在3 mM或25 mM K+培养基中孵育的切片中[3H]胆碱的乙酰化和摄取。刺激诱导的Ca2+内流略有抑制，即使在缺氧40分钟后仍为对照值的78.1%。与摄取过程相比，Ca2+依赖的神经递质释放过程本身似乎在缺氧情况下保存良好。我们的研究结果表明，缺氧可能根据神经传递突触前过程的特定敏感性导致神经活动的差异改变。
