Meric P, Barrere B, Peres M, Gillet B, Berenger G, Beloeil J C, Seylaz J
Laboratoire de Recherches Cérébrovasculaires, CNRS UA 641, Centre Universitaire Villemin, Paris, France.
Brain Res. 1994 Feb 28;638(1-2):53-60. doi: 10.1016/0006-8993(94)90632-7.
The cerebral metabolic changes elicited by kainate-induced seizures in the rat were investigated by in vivo combined NMR spectroscopy of 31P and 1H. Systemic injection of kainate induced no significant changes in cerebral ATP or PCr levels during up to 90 min of continuous, generalised seizures, and the cerebral 31P spectra showed only a transient mild cerebral acidosis 30 min after kainate administration. In parallel with the changes in intracellular cerebral pH, the 1H spectra showed a significant increase in lactate, which remained elevated throughout the seizures. These findings indicate that oxidative metabolism does not completely match the increased glycolysis during seizures though the energy homeostasis is maintained. This suggests that oxidative metabolism has a limited capacity to satisfy the brain's energy needs during the kainate-induced seizures, but that the different pathways of energy production in the brain cells can overcome this limitation. Thus the brain damage associated with this experimental model of epilepsy is not due to extended major failure of the energy supply.
通过对大鼠进行体内31P和1H联合核磁共振波谱分析，研究了红藻氨酸诱发的癫痫发作所引起的大脑代谢变化。全身性注射红藻氨酸，在长达90分钟的持续性全身性癫痫发作期间，大脑ATP或磷酸肌酸（PCr）水平未出现显著变化，并且大脑31P波谱显示，在注射红藻氨酸30分钟后仅出现短暂的轻度大脑酸中毒。与细胞内大脑pH值的变化同时出现的是，1H波谱显示乳酸显著增加，且在整个癫痫发作过程中一直保持升高。这些发现表明，尽管能量稳态得以维持，但癫痫发作期间氧化代谢并不能完全匹配增加的糖酵解。这表明，在红藻氨酸诱发的癫痫发作期间，氧化代谢满足大脑能量需求的能力有限，但脑细胞中不同的能量产生途径可以克服这一限制。因此，与这种癫痫实验模型相关的脑损伤并非由于能量供应的长期严重衰竭所致。
