Docherty M, Bradford H F, Anderton B, Wu J Y
FEBS Lett. 1983 Feb 7;152(1):57-61. doi: 10.1016/0014-5793(83)80481-5.
An antiserum to pure glutamate decarboxylase (GAD) when incubated with rat cortical synaptosomes in the presence of complement caused release of 33-53% of lactate dehydrogenase (LDH) and 22-41% of total GAD. In addition most of the gamma-aminobutyrate (GABA) present was released. Anti-GAD antiserum alone, or complement alone, were without action. The antiserum plus complement had no effect on noradrenaline or choline uptake, and did not release choline acetylase (ChAT). Anti-ChAT serum plus complement released 30-37% of ChAT and 10-13% of LDH. It prevented choline uptake. This serum did not produce GAD release or prevent GABA, choline or noradrenaline uptake. When cortical synaptosomes were exposed to both antisera plus complement, their actions were strictly additive. The data indicate specific lysis of GABAergic and cholinergic synaptosomal sub-populations.
将纯谷氨酸脱羧酶（GAD）抗血清与大鼠皮质突触体在补体存在的情况下一起孵育时，可导致33% - 53%的乳酸脱氢酶（LDH）以及22% - 41%的总GAD释放。此外，大部分存在的γ-氨基丁酸（GABA）也被释放。单独的抗GAD抗血清或单独的补体均无作用。抗血清加补体对去甲肾上腺素或胆碱摄取没有影响，也不释放胆碱乙酰转移酶（ChAT）。抗ChAT血清加补体可释放30% - 37%的ChAT和10% - 13%的LDH。它会阻止胆碱摄取。该血清不会导致GAD释放，也不会阻止GABA、胆碱或去甲肾上腺素的摄取。当皮质突触体同时暴露于两种抗血清加补体时，它们的作用严格相加。数据表明GABA能和胆碱能突触体亚群发生了特异性裂解。
