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本研究在发现溴氰菊酯（ＤＭ）可使突触前膜谷氨酸释放增加的基础上，探讨了ＤＭ对大鼠中枢神经系统不同部位的一氧化氮合成酶（ＮＯＳ）活性的影响。利用不同性质阻断剂，对影响ＮＯＳ活性的可能机理进行了研究。结果发现，ＤＭ可引起大脑皮层、海马及小脑部位的ＮＯＳ活性显著增加。Ｌ－硝基精氨酸是ＮＯＳ的竞争性抑制剂，它可抑制由ＤＭ所致ＮＯＳ活性的升高。尼莫地平是一种电压依赖性钙通道阻断剂，它也可以有效的抑制ＤＭ所致ＮＯＳ活性的增加。认为ＤＭ导致神经毒性的机理可能是通过谷氨酸过量释放，诱导ＮＯＳ活性的升高，造成神经元的损伤。
In this study, the effect of DM on the activity of nitric oxide synthase (NOS) in different parts of the central nervous system of rats was investigated based on the discovery that deltamethrin (DM) can increase glutamate release from the presynaptic membrane. The use of different types of blockers on the possible mechanism of NOS activity were studied. The results showed that DM can cause a significant increase in NOS activity in the cerebral cortex, hippocampus and cerebellum. L-nitroarginine is a competitive inhibitor of NOS that inhibits the elevation of NOS activity induced by DM. Nimodipine is a voltage-dependent calcium channel blocker that also effectively inhibits DM-induced increases in NOS activity. It is thought that the mechanism by which DM causes neurotoxicity may be due to excessive release of glutamate, inducing an increase in NOS activity and causing neuronal damage.