Scalzo F M, Newport G D, Gough B J, Ali S F, Holson R R
Division of Reproductive and Developmental Toxicology, National Center for Toxicological Research, Jefferson, Arkansas 72079.
Neurotoxicology. 1989 Fall;10(3):485-90.
Prenatal haloperidol exposure in rats is known to reduce striatal D2 receptor binding in postnatal day (PND) 30 offspring. The effects of prenatal haloperidol exposure on presynaptic dopamine (DA) autoreceptor function are not well described. Pregnant albino rats were given daily injections of haloperidol (2.5 or 5.0 mg/kg, sc) or vehicle over gestational days 6-20. Presynaptic DA autoreceptor function was assessed using the DOPA decarboxylase inhibitor NSD-1015 and gamma-butyrolactone in the caudate, nucleus accumbens and olfactory tubercles of male offspring sacrificed on PND 97. There appeared to be no impairment of autoreceptor function in any region studied. The data indicate that prenatal haloperidol exposure does not result in permanent alterations in presynaptic DA autoreceptor function.
已知大鼠产前接触氟哌啶醇会降低出生后第30天(PND 30)子代纹状体中的D2受体结合。产前接触氟哌啶醇对突触前多巴胺(DA)自身受体功能的影响尚无详尽描述。在妊娠第6至20天,对怀孕的白化大鼠每日注射氟哌啶醇(2.5或5.0 mg/kg,皮下注射)或赋形剂。在出生后第97天处死的雄性子代的尾状核、伏隔核和嗅结节中,使用多巴脱羧酶抑制剂NSD-1015和γ-丁内酯评估突触前DA自身受体功能。在所研究的任何区域中,自身受体功能似乎均未受损。数据表明,产前接触氟哌啶醇不会导致突触前DA自身受体功能发生永久性改变。