Allgaier C, Choi B K, Hertting G
Institute of Pharmacology and Toxicology, University of Freiburg, F.R.G.
J Neurochem. 1993 Sep;61(3):1043-9. doi: 10.1111/j.1471-4159.1993.tb03618.x.
[3H]Acetylcholine release elicited with 360 pulses/3 Hz from slices of rabbit hippocampus is facilitated in the presence of the muscarine (M) receptor antagonist atropine (indicating the existence of autoinhibition) and diminished by the M receptor agonists carbachol and oxotremorine. N-Ethylmaleimide (30 microM) and pertussis toxin (8 micrograms/ml) counteracted antagonist-induced facilitation and agonist-induced inhibition of release, suggesting that a pertussis toxin-sensitive GTP-binding protein is involved in the chain of events mediating activation of M receptors to inhibition of release. Neither 8-bromo-cyclic AMP (300 microM), a membrane analogue of cyclic AMP, nor rolipram (10 microM), a phosphodiesterase inhibitor, affected electrically evoked release of [3H]acetylcholine. They also did not influence the oxotremorine-induced inhibition of transmitter release. In conclusion, no evidence was found for the assumption that activation of M autoreceptors is linked to inhibition of adenylate cyclase.
在毒蕈碱(M)受体拮抗剂阿托品存在的情况下,以3赫兹频率施加360个脉冲刺激兔海马切片所引发的[3H]乙酰胆碱释放得到促进(表明存在自抑制作用),而M受体激动剂卡巴胆碱和氧化震颤素则使其减少。N - 乙基马来酰亚胺(30微摩尔)和百日咳毒素(8微克/毫升)可抵消拮抗剂诱导的释放促进作用和激动剂诱导的释放抑制作用,这表明一种对百日咳毒素敏感的GTP结合蛋白参与了介导M受体激活至释放抑制的一系列事件。环磷酸腺苷(cAMP)的膜类似物8 - 溴环磷酸腺苷(300微摩尔)和磷酸二酯酶抑制剂咯利普兰(10微摩尔)均不影响电诱发的[3H]乙酰胆碱释放。它们也不影响氧化震颤素诱导的递质释放抑制作用。总之,没有证据支持M自身受体激活与腺苷酸环化酶抑制相关的假设。