Fernandes M J, Dubé C, Boyet S, Marescaux C, Nehlig A
INSERM U 398, Université Louis Pasteur, Strasbourg, France.
J Cereb Blood Flow Metab. 1999 Feb;19(2):195-209. doi: 10.1097/00004647-199902000-00011.
The correlation between seizure-induced hypermetabolism and subsequent neuronal damage was studied in 10-day-old (P10), 21-day-old (P21), and adult rats subjected to lithium-pilocarpine status epilepticus (SE). Local CMRglc (LCMRglc) values were measured by the [14C]2-deoxyglucose method for a duration of 45 minutes starting at 60 minutes after the onset of SE, and neuronal damage was assessed by cresyl violet staining at 6 days after SE. In P21 and adult rats, LCMRglc values were increased by 275 to 875% in all thalamic, cortical, forebrain, and hypothalamic regions plus the substantia nigra. In addition, at P21 there were also large increases in LCMRglc in brainstem regions. In P10 rats, metabolic increases were mostly located in cortical and forebrain regions plus the substantia nigra but did not affect hypothalamic, thalamic, or brainstem areas. In adult rats, there was an anatomical correlation between hypermetabolism and neuronal damage. At P21, although hypermetabolism occurred in regions with damage, the extent of damage varied considerably with the animals and ranged from an almost negligible to a very extended degree. Finally, in P10 rats, although quite pronounced hypermetabolism occurred, there was no neuronal damage induced by the seizures. Thus, in the present model of epilepsy, the correlation between marked hypermetabolism and neuronal damage can be shown in adult rats. Conversely, immature rats can sustain major metabolic activations that lead either to a variable extent of damage, as seen at P21, or no damage, as recorded at P10.
在遭受锂-匹罗卡品诱导的癫痫持续状态（SE）的10日龄（P10）、21日龄（P21）和成年大鼠中，研究了癫痫发作诱导的代谢亢进与随后神经元损伤之间的相关性。从SE发作后60分钟开始，采用[14C]2-脱氧葡萄糖法持续45分钟测量局部脑葡萄糖代谢率（LCMRglc）值，并在SE发作后6天通过甲酚紫染色评估神经元损伤。在P21和成年大鼠中，所有丘脑、皮质、前脑、下丘脑区域以及黑质的LCMRglc值增加了275%至875%。此外，在P21时，脑干区域的LCMRglc也大幅增加。在P10大鼠中，代谢增加主要位于皮质、前脑区域以及黑质，但未影响下丘脑、丘脑或脑干区域。在成年大鼠中，代谢亢进与神经元损伤之间存在解剖学相关性。在P21时，尽管损伤区域出现代谢亢进，但损伤程度在不同动物之间差异很大，范围从几乎可以忽略不计到非常广泛。最后，在P10大鼠中，尽管出现了相当明显的代谢亢进，但癫痫发作并未诱导神经元损伤。因此，在目前的癫痫模型中，成年大鼠可显示出明显的代谢亢进与神经元损伤之间的相关性。相反，未成熟大鼠能够承受主要代谢激活，这要么导致不同程度的损伤（如P21所见），要么不导致损伤（如P10记录）。
