Boyes W K, Moser V C
Neurotoxicology Division, United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711.
Toxicol Appl Pharmacol. 1988 Mar 15;92(3):402-18. doi: 10.1016/0041-008x(88)90180-9.
The hypothesis that chlordimeform increased the amplitude of components N1P1 and P1N3 in rat pattern-reversal visual evoked potentials through actions on alpha 2-adrenergic receptors was tested with two sets of experiments. First, rats received single injections of either vehicle, an alpha 2-adrenergic antagonist yohimbine (0.1, 0.5, or 2.0 mg/kg), or an alpha 2-adrenergic agonist clonidine (0.05, 0.1, or 0.5 mg/kg). Yohimbine alone had no effect on pattern-reversal evoked potential amplitude. Clonidine treatment produced a dosage related increase in amplitude of both components similar to that produced by chlordimeform (W.K. Boyes and R.S. Dyer, 1984, Brain Res. Bull., 10, 817-823). Second, rats were given double injections of either vehicle or yohimbine (0.05, 0.5, 2.0, or 5.0 mg/kg) followed by either vehicle, clonidine (0.1 or 0.2 mg/kg) or chlordimeform (10, 20, or 40 mg/kg). Yohimbine pretreatment attenuated the effects of subsequent treatment with either clonidine or chlordimeform. These results support the hypothesis that chlordimeform alters rat pattern-reversal evoked potentials through actions as a central nervous system alpha 2-adrenergic agonist.
通过两组实验对杀虫脒通过作用于α2-肾上腺素能受体增加大鼠图形翻转视觉诱发电位中N1P1和P1N3成分波幅这一假说进行了验证。首先，给大鼠单次注射溶剂、α2-肾上腺素能拮抗剂育亨宾（0.1、0.5或2.0毫克/千克）或α2-肾上腺素能激动剂可乐定（0.05、0.1或0.5毫克/千克）。单独使用育亨宾对图形翻转诱发电位波幅没有影响。可乐定处理使两个成分的波幅呈剂量相关增加，类似于杀虫脒所产生的增加（W.K.博伊斯和R.S.戴尔，1984年，《脑研究通报》，10，817 - 823）。其次，给大鼠双次注射溶剂或育亨宾（0.05、0.5、2.0或5.0毫克/千克），随后再注射溶剂、可乐定（0.1或0.2毫克/千克）或杀虫脒（10、20或40毫克/千克）。育亨宾预处理减弱了随后用可乐定或杀虫脒处理的效果。这些结果支持了杀虫脒作为中枢神经系统α2-肾上腺素能激动剂通过其作用改变大鼠图形翻转诱发电位的假说。
