Johnson G V, Hartzell C R
Anesth Analg. 1985 Apr;64(4):395-9.
Synaptosomes isolated from rat cerebra were used as a model to study the effects of halothane on choline uptake and acetylcholine synthesis and release processes. Synaptosomes are membrane-bound particles that are formed by gentle disruption of brain tissue. These particles include the presynapse, cleft, portions of postsynaptic membrane, and all other components contained in brain nerve terminals necessary for neurotransmitter synthesis, storage, and release. Halothane (3% in air, vol/vol) caused a "competitive-like" inhibition of choline uptake in synaptosomes but had no effect on the enzymatic activity of choline acetyl-transferase (ChAT). Three percent halothane depressed synaptosomal acetylcholine (ACh) synthesis by 86% while ACh release from synaptosomes was inhibited 50%. It is suggested that halothane inhibits ACh synthesis by directly interfering with the carrier-mediated transport system of choline. Since halothane also inhibits ACh release, as well as choline uptake, it is probable that the anesthetic is acting upon more than one site in these cholinergic nerve terminals. These data require an interpretive evaluation that cannot fit the "unitary" hypothesis as the mechanism of action of general anesthetics.
从大鼠大脑中分离出的突触体被用作模型，以研究氟烷对胆碱摄取、乙酰胆碱合成和释放过程的影响。突触体是通过轻柔破坏脑组织形成的膜结合颗粒。这些颗粒包括突触前膜、突触间隙、部分突触后膜以及神经递质合成、储存和释放所需的脑神经末梢中包含的所有其他成分。氟烷（空气中体积分数为3%）对突触体中胆碱摄取产生“竞争性”抑制，但对胆碱乙酰转移酶（ChAT）的酶活性没有影响。3%的氟烷使突触体乙酰胆碱（ACh）合成降低86%，而突触体中ACh释放受到50%的抑制。提示氟烷通过直接干扰胆碱的载体介导转运系统来抑制ACh合成。由于氟烷还抑制ACh释放以及胆碱摄取，麻醉剂很可能作用于这些胆碱能神经末梢的多个位点。这些数据需要进行解释性评估，而不能将“单一”假说作为全身麻醉药的作用机制。
