巴金森氏症主要是中腦A9區多巴胺神經產生退化,而其他的神經傳導物質也發生相對的改變,其中substance P(SP)所扮演的調控功能,更受到研究者的注意。多巴胺神經對SP之調控,可利用6-OHDA(6-hydroxydopamine)或MPTP(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)破壞多巴胺神經,以及利用多巴胺之作用劑或拮抗劑來觀察SP之變化,大多數的研究發現SP之神經活性,隨多巴胺之變化而有平行性的改變,當多巴胺的功能減少,SP之神經活性也隨之降低,反之亦然。至於SP神經對多巴胺之調控,在離體實驗中,SP可促進黑質以及紋狀體多巴胺的釋放,但在活體的實驗中,由於SP之藥理特性,而有不一致的研究報告,但整體而言,大多數的研究者較支持,SP對多巴胺之活性有正性加強之作用,換言之,在黑質或紋狀體SP的給與,可增加多巴胺之釋放功能。
The etiology of the Parkinson's disease is believed to be a deficiency in dopaminergic (DA-ergic) functions in the A9 area of the central nervous system, as well as the change of other neurotransmitters in the brain. Considering the multiple dynamic changes, the substance P (SP) possessed the important modulation function in the DA system. DA neuron may modulate the SP neuron, after lesion the DA neuron either with the 6-OHDA (6-hydrodopamine) or MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), as well as using the DA agonist or antagonist, the SP neuron activity would accordingly change by the DA neuron, vise visa. Moreover, the DA neuron also change it's activity by the SP administration in vitro and in vivo study. Although, because of the desensitization property of SP, some of the reports showed the inconsistency results, however, most of the researches support the concept that SP has the positive effects on DA neuron. In conclusion, DA and SP neurons parallel modulate each other with the positive feed back effect.