Doctor S V, Costa L G, Kendall D A, Murphy S D
Toxicology. 1982;25(2-3):213-21. doi: 10.1016/0300-483x(82)90031-2.
Trimethyltin (TMT), in a concentration dependent manner, inhibits in vitro uptake of gamma-aminobutyric acid (GABA), norepinephrine and serotonin by mouse forebrain synaptosomes with IC50S of 75, 43 and 24 microM, respectively. At 2 h and 14 h following in vivo administration of TMT (4.26 mg/kg; i.p.) to mice, GABA and serotonin uptake by forebrain synaptosomes are decreased, although norepinephrine uptake was not significantly affected. In vitro kinetic analyses of TMT inhibition of forebrain synaptosomal uptake of GABA, norepinephrine and serotonin indicated that the inhibition was not of the competitive type. This inhibition of uptake of neurotransmitters could be responsible, at least in part, for altered neurotransmitter levels in the synaptic cleft and may contribute to altered nervous system function during TMT intoxication.
三甲基锡（TMT）以浓度依赖的方式抑制小鼠前脑突触体对γ-氨基丁酸（GABA）、去甲肾上腺素和5-羟色胺的体外摄取，其半数抑制浓度（IC50）分别为75、43和24微摩尔。给小鼠腹腔注射TMT（4.26毫克/千克）后2小时和14小时，前脑突触体对GABA和5-羟色胺的摄取减少，而去甲肾上腺素的摄取未受显著影响。对TMT抑制前脑突触体摄取GABA、去甲肾上腺素和5-羟色胺的体外动力学分析表明，这种抑制并非竞争性抑制。神经递质摄取的这种抑制可能至少部分地导致突触间隙中神经递质水平的改变，并可能在TMT中毒期间导致神经系统功能改变。
