Haskel Y, Hanani M
Laboratory of Experimental Surgery, Hadassah University Hospital, Mount Scopus, Jerusalem, Israel.
Dig Dis Sci. 1994 Nov;39(11):2364-7. doi: 10.1007/BF02087652.
The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was injected intraperitoneally in mice and caused an acute inhibition (of over 60%) of gastrointestinal motility, which was measured by the transit of charcoal. This inhibition was not related to conversion of MPTP to MPP+. Administration of the beta-adrenergic blocker propranolol significantly reduced, but did not completely block, the effect of MPTP. The dopaminergic blocker haloperidol also partly reversed the effects of MPTP. When these blockers were administered together, the action of MPTP was fully blocked. The results indicate that the toxin acted by releasing catecholamines (presumably norepinephrine and dopamine), thereby inhibiting motility.
将神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)腹腔注射到小鼠体内,导致胃肠蠕动急性抑制(超过60%),胃肠蠕动通过炭末传输来测定。这种抑制与MPTP转化为MPP⁺无关。给予β-肾上腺素能阻滞剂普萘洛尔可显著降低但未完全阻断MPTP的作用。多巴胺能阻滞剂氟哌啶醇也部分逆转了MPTP的作用。当这些阻滞剂一起给药时,MPTP的作用被完全阻断。结果表明,该毒素通过释放儿茶酚胺(可能是去甲肾上腺素和多巴胺)起作用,从而抑制蠕动。