Gardner C R, Richards M H
Brain Res. 1981 Jul 20;216(2):291-8. doi: 10.1016/0006-8993(81)90131-1.
Mice treated with D,L-alpha-monofluoromethyl-dopa (MFMD, RMI 71963), an irreversible inhibitor of aromatic L-amino acid decarboxylase (AADC), showed marked decrease in whole-brain concentrations of norepinephrine, dopamine and serotonin. The recovery of these concentrations to control values was slower than would be predicted on the basis of the activity of AADC measured in whole-brain homogenates. Subcellular fractionation of brain homogenates prepared from mice treated with MFMD showed that at least two pools of AADC activity could be distinguished by differences in their recovery rates. In the synaptosomal pool, which represents the nerve terminal AADC, the recovery of enzyme activity was significantly delayed with respect to the non-synaptosomal pool. These findings can be explained on the basis of enzyme synthesis within the nerve cell bodies and subsequent axonal transport to the nerve terminals which are the major sites of neurotransmitter synthesis.
用芳香族L-氨基酸脱羧酶（AADC）的不可逆抑制剂D，L-α-单氟甲基多巴（MFMD，RMI 71963）处理的小鼠，其全脑去甲肾上腺素、多巴胺和5-羟色胺浓度显著降低。这些浓度恢复到对照值的速度比根据全脑匀浆中测得的AADC活性所预测的要慢。对用MFMD处理的小鼠制备的脑匀浆进行亚细胞分级分离表明，至少可以通过AADC活性恢复率的差异区分出两个酶活性池。在代表神经末梢AADC的突触体池中，酶活性的恢复相对于非突触体池明显延迟。这些发现可以基于神经细胞体内的酶合成以及随后轴突运输到作为神经递质合成主要部位的神经末梢来解释。
