Bodnar R J, Merrigan K P, Wallace M M
Pharmacol Biochem Behav. 1981 Apr;14(4):579-81. doi: 10.1016/0091-3057(81)90321-x.
The glucose analogue, 2-deoxy-D-glucose (2-DG) elicits hyperphagic and analgesic responses in rats. The former response appears to be mediated by central processes since overeating is elicited following intraventricular administration of 2-DG at low (3.5 and 5.0 mg/kg) doses. The present study examined whether flinch-jump threshold would increase 30, 90 and 180 min following intraventricular injections of 2-DG at low (3.5, 5.0 and 10.0 mg/kg) doses and compared these effects with systemically-applied 2-DG doses of 350 and 500 mg/kg. Intraventricular 2-DG administration increased jump thresholds for up to 180 min across all test doses. Flinch thresholds were also increased, but in a manner dissociated from jump thresholds. Animals with cannulae located near, but not in the lateral ventricle, displayed delayed analgesic effects. The magnitude of intraventricular 2-DG analgesia was not at potent as the 100-fold higher systemic injections. It appears that central mechanisms mediated intraventricular 2-DG analgesia at the low dose range since higher, systemic 2-DG doses have previously failed to increase flinch-jump thresholds.
葡萄糖类似物2-脱氧-D-葡萄糖(2-DG)在大鼠中会引发摄食亢进和镇痛反应。前一种反应似乎是由中枢过程介导的,因为在脑室内注射低剂量(3.5和5.0毫克/千克)的2-DG后会引发暴饮暴食。本研究考察了在脑室内注射低剂量(3.5、5.0和10.0毫克/千克)的2-DG后30、90和180分钟退缩跳跃阈值是否会升高,并将这些效应与全身应用350和500毫克/千克的2-DG剂量进行比较。在所有测试剂量下,脑室内注射2-DG均可使跳跃阈值升高长达180分钟。退缩阈值也有所升高,但方式与跳跃阈值不同。插管位于侧脑室附近但不在侧脑室内的动物表现出延迟的镇痛作用。脑室内注射2-DG的镇痛强度不如高100倍的全身注射。由于更高的全身2-DG剂量此前未能提高退缩跳跃阈值,因此似乎中枢机制介导了低剂量范围内脑室内注射2-DG的镇痛作用。