Depaulis A, Vergnes M
Psychopharmacology (Berl). 1984;83(4):367-72. doi: 10.1007/BF00428547.
When GABA-potentiating compounds were administered IP to rats with prior experience of mouse-killing behaviour, a reduction of killing was observed with gamma-vinyl GABA (200 and 400 mg/kg) and nipecotic acid amide (400 mg/kg), while no significant effect was noted following injection of dipropylacetate or THIP. The inhibitory effects of gamma-vinyl GABA and nipecotic acid amide were not reversed by subsequent injection of picrotoxin and were associated with sedation as observed in open field and actograph tests. When GABA-potentiating compounds were administered to food-deprived rats exposed for the first time to a mouse (initial elicitation), administration of gamma-vinyl GABA, dipropylacetate, nipecotic acid amide or THIP increased the incidence of mouse-killing behaviour. Conversely, the incidence of mouse-killing under the same conditions was reduced following injections of picrotoxin. These results do not support the hypothesis that the general activation of GABAergic mechanisms inhibits mouse-killing behaviour in rats. On the contrary, data obtained in naive animals suggest that potentiation of these mechanisms actually facilitates the initial elicitation of this behaviour.
当向有捕杀小鼠行为经验的大鼠腹腔注射γ-氨基丁酸增强化合物时,观察到γ-乙烯基γ-氨基丁酸(200和400毫克/千克)和烟碱酸酰胺(400毫克/千克)可减少捕杀行为,而注射二丙基乙酸酯或四氢异喹啉后未观察到显著效果。γ-乙烯基γ-氨基丁酸和烟碱酸酰胺的抑制作用不会因随后注射印防己毒素而逆转,并且与旷场试验和活动记录试验中观察到的镇静作用有关。当向首次接触小鼠(初始诱发)的饥饿大鼠施用γ-氨基丁酸增强化合物时,γ-乙烯基γ-氨基丁酸、二丙基乙酸酯、烟碱酸酰胺或四氢异喹啉的施用增加了捕杀小鼠行为的发生率。相反,在相同条件下,注射印防己毒素后捕杀小鼠的发生率降低。这些结果不支持γ-氨基丁酸能机制的普遍激活会抑制大鼠捕杀小鼠行为的假设。相反,在未经处理的动物中获得的数据表明,这些机制的增强实际上促进了这种行为的初始诱发。