Jackisch R, Strittmatter H, Kasakov L, Hertting G
Naunyn Schmiedebergs Arch Pharmacol. 1984 Oct;327(4):319-25. doi: 10.1007/BF00506243.
Modulation of acetylcholine release via adenosine receptors was studied in rabbit hippocampal slices, which were preincubated with 3H-choline and then continuously superfused. Electrical field stimulation of the slices elicited a release of acetylcholine, which was inhibited in a concentration-dependent manner by various adenosine receptor agonists. The effects of the agonists were antagonized by the methylxanthines. From the order of potency: cyclohexyladenosine greater than (-)phenylisopropyladenosine [-)PIA) greater than 5'-N-ethylcarboxamideadenosine (NECA) greater than 2-chloradenosine greater than (+)phenylisopropyladenosine greater than adenosine, the inhibitory adenosine receptor may be classified as A1-(R1-)receptor. In experiments on rabbit caudate nucleus slices, adenosine receptor agonists only slightly decreased the evoked acetylcholine release. The presence of an inhibitory tone of endogenous adenosine on hippocampal acetylcholine release is supported by the following findings: 1) the methylxanthines theophylline, 8-phenyltheophylline and 3-isobutylmethylxanthine (IBMX) increased the evoked acetylcholine release in concentrations below those required for phosphodiesterase inhibition. 2) Adenosine uptake inhibitors, in contrast, decreased the evoked transmitter release. 3) Deamination of endogenous adenosine by addition of adenosine deaminase to the medium enhanced the acetylcholine release. In conclusion, acetylcholine release in the hippocampus is depressed at the level of the cholinergic nerve terminals by endogenous adenosine via A1-(R1-)receptors.
在预先用³H-胆碱孵育然后持续灌流的兔海马切片中研究了通过腺苷受体对乙酰胆碱释放的调节。对切片进行电场刺激可引起乙酰胆碱释放,各种腺苷受体激动剂以浓度依赖性方式抑制该释放。激动剂的作用被甲基黄嘌呤拮抗。根据效力顺序:环己基腺苷大于(-)苯异丙基腺苷[(-)PIA]大于5'-N-乙基甲酰胺腺苷(NECA)大于2-氯腺苷大于(+)苯异丙基腺苷大于腺苷,抑制性腺苷受体可分类为A1-(R1-)受体。在兔尾状核切片实验中,腺苷受体激动剂仅轻微降低诱发的乙酰胆碱释放。内源性腺苷对海马乙酰胆碱释放存在抑制性调节作用得到以下发现的支持:1)甲基黄嘌呤茶碱、8-苯基茶碱和3-异丁基甲基黄嘌呤(IBMX)在低于磷酸二酯酶抑制所需浓度时增加诱发的乙酰胆碱释放。2)相反,腺苷摄取抑制剂降低诱发的递质释放。3)通过向培养基中添加腺苷脱氨酶对内源性腺苷进行脱氨增强了乙酰胆碱释放。总之,内源性腺苷通过A1-(R1-)受体在胆碱能神经末梢水平抑制海马中的乙酰胆碱释放。