LONG-TERM EFFECTS OF INTRA-HIPPOCAMPAL KAINIC ACID INJECTION IN RATS - A METHOD FOR INDUCING SPONTANEOUS RECURRENT SEIZURES

LONG-TERM EFFECTS OF INTRA-HIPPOCAMPAL KAINIC ACID INJECTION IN RATS - A METHOD FOR INDUCING SPONTANEOUS RECURRENT SEIZURES
复制标题

DOI:
10.1016/0013-4694(82)90134-1
复制
发表时间:
1982-01-01
期刊:
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY
影响因子:
--
通讯作者:
LASALLE, GL
LASALLE, GL
中科院分区:
其他
文献类型:
--
作者:
CAVALHEIRO, EA;RICHE, DA;LASALLE, GL

文献摘要

被引文献

相似文献

红藻氨酸(KA)是一种强效的惊厥剂和神经毒剂。当大脑内给药时,它会导致.apprx反复发作。一到两天,局部和几个偏远的脑区都有脑损伤。本文报道了海马内注射KA的远期疗效。在Wistar大鼠的右侧海马区注射0.1~3.0ug的KA,并在一段时间内观察其行为和脑电。3个月。在0.8-2.0µg的KA剂量后,观察到4个不同的阶段:持续1-2天的急性期,与已描述的重复发作模式相对应;静止期(5-21天),其特征是逐渐恢复到明显正常的脑电和行为,除了接受最高剂量的动物的一些攻击行为;自发反复发作阶段(这些发作始于注射KA后6-22天,主要在处理和复发时触发)。.apprx每天2次。30天;它们通常类似于杏仁核点燃的癫痫发作);癫痫发作后阶段,没有观察到更多的癫痫发作,但在杏仁核记录中可以看到显著的尖峰活动。接受0.1-0.4微克KA剂量的动物没有超过急性期,而接受3.0微克KA剂量的动物在第一阶段死亡。神经病理检查显示剂量依赖性改变。这些系列事件为诱发自发性反复发作伴脑损伤提供了一种新的方法。
Kainic acid (KA) is known as a powerful convulsant and neurotoxic agent. When intracerebrally administered it causes repetitive seizures for .apprx. 1 or 2 days and brain damage both locally and in several remote brain regions. The long-term effects of intrahippocampal KA administration are reported. Doses from 0.1-3.0 .mu.g of KA were injected in the right hippocampus of Wistar rats, and both the behavior and EEG were observed during a period of .apprx. 3 mo. Following KA doses of 0.8-2.0 .mu.g, 4 distinct phases wee observed; an acute phase which lasted 1-2 days and corresponded to the pattern of repetitive seizures already described; silent phase (5-21 days) which was characterized by a progressive return to apparently normal EEG and behavior, except for some aggressive behavior in animals receiving the highest doses; phase of spontaneous recurrent seizures (these seizures started 6-22 days after KA injections and were mostly triggered upon handling and recurred .apprx. 2 times a day for .apprx. 30 days ; usually they resembled the amygdaloid kindled seizures); and a postseizure phase where no more seizures were observed but significant spiking activity in the amygdala recordings was seen. Animals receiving KA doses of 0.1-0.4 .mu.g did not evolve beyond the acute phase whereas those receiving 3.0 .mu.g died during this 1st phase. Neuropathological examination revealed dose-dependent alterations. These serial events offer a new method to induce spontaneous recurrent seizures with brain damage.