Shephard R A, Stevenson D, Jenkinson S
Psychopharmacology (Berl). 1985;86(3):313-7. doi: 10.1007/BF00432220.
The effects of valproate (30-500 mg/kg), alone and in combination with picrotoxin (1.5 mg/kg) or RO 15-1788 (10 mg/kg) were studied in two experiments on hyponeophagia in rats. Valproate reduced eating latency and increased eating time and amount eaten of novel food, except at 500 mg/kg which reduced feeding. Picrotoxin induced generally opposite actions alone and shifted valproate dose/response curves to the right. RO 15-1788 had no detectable intrinsic action, but prevented both the behavioural facilitation and inhibition produced by valproate. These findings are discussed in the context of the GABA hypothesis of benzodiazepine action, with the conclusions that they provide behavioural support for the hypothesis of a receptor complex with GABA and benzodiazepine binding sites, and that an optimal and submaximal level of activity at the benzodiazepine site is a necessary condition for anxiolytic actions of valproate.
在两项关于大鼠食欲减退的实验中，研究了丙戊酸盐（30 - 500毫克/千克）单独使用以及与印防己毒素（1.5毫克/千克）或RO 15 - 1788（10毫克/千克）联合使用的效果。丙戊酸盐可缩短进食潜伏期，增加对新食物的进食时间和进食量，但500毫克/千克剂量时会减少进食。印防己毒素单独使用时通常产生相反的作用，并将丙戊酸盐的剂量/反应曲线向右移动。RO 15 - 1788没有可检测到的内在作用，但可阻止丙戊酸盐产生的行为促进和抑制作用。这些发现是在苯二氮䓬作用的GABA假说背景下进行讨论的，得出的结论是，它们为存在GABA和苯二氮䓬结合位点的受体复合物假说提供了行为支持，并且苯二氮䓬位点的最佳和次最大活性水平是丙戊酸盐抗焦虑作用的必要条件。
