地西泮对红藻氨酸处理大鼠脑葡萄糖利用的减弱作用。

Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam.

作者信息

Chastain J E, Samson F, Nelson S R, Pazdernik T L

机构信息

Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, College of Health Sciences, Kansas City 66103.

出版信息

Eur J Pharmacol. 1987 Oct 13;142(2):215-24. doi: 10.1016/0014-2999(87)90110-5.

DOI:10.1016/0014-2999(87)90110-5

PMID:3691639

Abstract

Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself.

摘要

通过定量[14C]2-脱氧葡萄糖法评估地西泮对 kainic 酸诱发癫痫发作所致局部脑葡萄糖利用（LCGU）的影响。在测定 LCGU 前 3 小时或 48 小时，给雄性大鼠腹腔注射 kainic 酸（12mg/kg）或其溶剂。在 kainic 酸注射前 15 分钟、注射后 1 小时和 2.5 小时，给大鼠肌肉注射地西泮（3.2mg/kg）或其溶剂。地西泮可阻断 kainic 酸诱发的明显惊厥，在 3 小时时减弱 LCGU 的增加，并防止梨状皮质和杏仁核在 48 小时时 LCGU 的降低。在 3 小时地西泮-kainic 酸组中，海马体的 CA3（438%）、CA4（537%）和 CA1-腹侧（340%）、脚间核（200%）和外侧丘系（213%）的 LCGU（相对于溶剂的百分比）仍显著高于溶剂组水平。这些结果表明，地西泮可抑制 kainic 酸诱发的癫痫活动从假定的 CA3 致痫灶的扩散。此外，地西泮可降低但不能消除病灶本身的高代谢活动。