Tremblay E, Ottersen O P, Rovira C, Ben-Ari Y
Neuroscience. 1983;8(2):299-315. doi: 10.1016/0306-4522(83)90068-4.
Kainic acid was injected unilaterally in the amygdala of the rat. Following various delays, 2-deoxy-D-[14C]glucose was given intravenously. Autoradiographs of frontal brain sections showed increased glucose uptake in a number of cerebral structures as compared with controls. Most of these structures belong to, or are closely related to, what is traditionally called the 'limbic system'. The structures that show an increased glucose consumption subsequent to kainic acid injections are, with few exceptions, identical to those that are sensitive to the toxic effect that kainic acid exerts on structures distant to the site of injection. The findings are discussed in relation to the hypothesis that the latter effect is secondary to the epileptogenic properties of kainic acid.
将海藻酸单侧注射到大鼠杏仁核中。经过不同时间的延迟后,静脉注射2-脱氧-D-[14C]葡萄糖。额叶脑切片的放射自显影片显示,与对照组相比,多个脑结构中的葡萄糖摄取增加。这些结构中的大多数属于或紧密相关于传统上所称的“边缘系统”。注射海藻酸后显示葡萄糖消耗增加的结构,除少数例外,与那些对海藻酸对注射部位远处结构产生的毒性作用敏感的结构相同。结合海藻酸的致癫痫特性导致后一种作用这一假说对这些发现进行了讨论。