Role of nitric oxide and glutamate in methamphetamine-induced psychosis

反复滥用甲基苯丙胺可导致人类出现精神分裂症样精神病，并对动物产生行为致敏和神经毒性。了解MA的神经药理学可能有助于了解MA诱发的精神病和精神分裂症的发病机制。本研究探讨了一氧化氮（NO）合成在MA行为致敏和MA诱导的神经毒性中的作用。1) NO合成酶抑制剂可降低单次给药诱导的行为改变。2)NO合成酶抑制剂对ma诱导的纹状体DA释放无影响。3) NO合成酶抑制剂降低了ma诱导的刻板印象的致敏程度。4) NO合成酶抑制剂可减弱ma诱导的纹状体多巴胺能神经毒性。综上所述，这些结果表明NO合成在MA诱导的急性行为改变和MA行为敏化的发展中起作用。此外，NO合成被认为与ma诱导的神经毒性有关。

Repeated abuse of methamphetamine (MA) results in schizophrenia-like psychosis in human, and this abuse produces behavioral sensitization and neurotoxicity in animals. Understanding of neuropharmacology of MA may provide insight into the pathogenesis of both MA-induced psychosis and schizophrenia. This research examined a role of nitric oxide (NO) synthesis in behavioral sensitization to MA and MA-induced neurotoxicity.1) NO synthase inhibitor reduced the behavioral changes induced by a single administration of MA.2) NO synthase ingibitor had no effect on MA-induced DA release in the striatum.3) NO synthase inhibitor reduced the degree of the sensitization to MA-induced stereotypy.4) NO synthase inhibitor attenuated the MA-induced dopaminergic neurotoxicity in the striatum.Taken together, these results suggest that NO synthesis play a role in MA-induced acute behavioral changes and the development of behavioral sensitization to MA.Furthermore, NO synthesis has been suggested to be related to MA-induced neurotoxicity.