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首页> 外文期刊>Life sciences >Low concentrations of methamidophos do not alter AChE activity but modulate neurotransmitters uptake in hippocampus and striatum in vitro.
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Low concentrations of methamidophos do not alter AChE activity but modulate neurotransmitters uptake in hippocampus and striatum in vitro.

机译：低浓度的甲胺磷不会改变AChE活性，但会在体外调节海马和纹状体中神经递质的摄取。

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AIMS: Methamidophos (Meth) is a toxic organophosphorus compound (OP) that inhibits acetylcholinesterase enzyme (AChE) and induces neurotoxicity. As the mechanism of its neurotoxic effects is not well understood, the aim of the present study was to evaluate the effects of Meth on glutamate and gamma aminobutyric acid (GABA) uptake and correlate with cell viability and AChE and Na(+)/K(+)-ATPase enzyme activities in striatum and hippocampus slices exposed to low concentrations (0.05 to 1.0 muM) of Meth. MAIN METHODS: Hippocampal and striatal slices of rat brain were exposed to Meth for 5 min ([(3)H]Glutamate uptake) or 15 min ([(3)H]GABA uptake) for assays. The enzyme activities and cell viability were also accessed at both times in hippocampal and striatal slices and homogenates. KEY FINDINGS: At concentrations that did not inhibit AChE, Meth caused changes in glutamate uptake in striatal (0.05 and 1.0 muM Meth) and hippocampal (1.0 muM Meth) slices. GABA uptake was increased by the pesticide in striatum at 0.5 and 1.0 muM and in hippocampus at 0.05 muM. After 3.5h of Meth exposure, striatal and hippocampal cells showed no changes in viability as well as no inhibition of Na(+)/K(+)-ATPase were observed after 5 or 15 min exposure to Meth in the same brain structures. SIGNIFICANCE: Results suggest that Meth, even without changing the AChE activity can modify somehow the neurotransmitters uptake. However, further studies are necessary to clarify if this modulation in glutamate or GABA uptake may be responsible to cause some disturbance in behavior or in other neurochemical parameters following low Meth exposure in vivo.
机译：目的：甲胺磷（Meth）是一种有毒的有机磷化合物（OP），可抑制乙酰胆碱酯酶（AChE）并引起神经毒性。由于尚不清楚其神经毒性作用的机制，因此本研究的目的是评估甲基苯丙氨酸对谷氨酸和γ-氨基丁酸（GABA）吸收的影响，并与细胞活力以及AChE和Na（+）/ K（暴露于低浓度（0.05至1.0μM）的Meth的纹状体和海马切片中的+）-ATPase酶活性主要方法：将大鼠脑的海马和纹状体切片暴露于Meth 5分钟（[[3] H]谷氨酸摄取）或15分钟（[[3] H] GABA摄取）进行检测。在海马和纹状体切片和匀浆中，酶活性和细胞活力也同时获得。主要发现：在不抑制AChE的浓度下，Meth引起纹状体（0.05和1.0μMMeth）和海马（1.0μMMeth）切片的谷氨酸吸收变化。纹状体中的农药分别以0.5和1.0μM以及海马中的GABA吸收为0.05μM来增加。甲基苯丙胺暴露3.5h后，纹状体和海马细胞在相同的大脑结构中暴露于甲基苯丙胺5或15分钟后未观察到活力变化，也未观察到Na（+）/ K（+）-ATPase抑制作用。意义：结果表明，即使不改变AChE活性，甲基也可以通过某种方式改变神经递质的摄取。但是，有必要进行进一步的研究以阐明谷氨酸或GABA摄取的这种调节是否可能导致体内低甲基硫磷暴露后行为或其他神经化学参数的某些紊乱。

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