Agnati L F, Fuxe K, Benfenati F, Battistini N, Zini I, Toffano G
Neurosci Lett. 1983 Oct 10;40(3):293-7. doi: 10.1016/0304-3940(83)90054-x.
Chronic ganglioside treatment (10 mg/kg, i.p.) using the molecular species with only one neuroaminic acid residue (GM1) given together with haloperidol (0.3 and 5 mg/kg, i.p.) once daily in male rats, counteracted the haloperidol-induced increase in the number of [3H]spiperone binding sites in striatal membranes when the low dose of haloperidol, but not the high dose, was administered. The present results therefore indicate that chronic GM1 treatment can partially counteract the increase in the number of dopamine receptors having a high affinity for neuroleptics (D2 type) induced by chronic haloperidol treatment in striatal membranes, and therefore may also partially counteract the development of neuroleptic-induced dopamine receptor supersensitivity.
在雄性大鼠中,每天一次腹腔注射仅含一个神经氨酸残基的神经节苷脂分子种类(GM1,10毫克/千克),同时腹腔注射氟哌啶醇(0.3和5毫克/千克),当给予低剂量而非高剂量氟哌啶醇时,可抵消氟哌啶醇诱导的纹状体膜中[3H]司哌罗宁结合位点数量增加。因此,目前的结果表明,慢性GM1治疗可部分抵消慢性氟哌啶醇治疗诱导的纹状体膜中对神经阻滞剂具有高亲和力的多巴胺受体(D2型)数量增加,因此也可能部分抵消神经阻滞剂诱导的多巴胺受体超敏反应的发展。