EPILEPTIC NEURONAL ACTIVITY & HIPPOCAMPAL DAMAGE

已经开发了一个实验模型来研究功能 和癫痫发作活动的结构后果，并阐明 海马体的正常结构和功能 扣押 海马体的活动，这发生在人类的颞叶 癫痫病的症状有哪些？ 癫痫，一种持续性癫痫放电的情况，通常是 与海马损伤的特征模式有关。 这种损伤模式可以在正常动物中复制， 电刺激穿通通路，主要传入神经 通往海马体的通路 刺激动物并允许其 可以使用各个时段的恢复来确定更改 在功能和结构上， 活动 这些动物因此构成了一个方面的模型 癫痫状态，即反复发作的影响。 设计了实验来确定 选择性神经元丢失和观察到的两种变化之间的关系， 剩余神经元的兴奋性和抑制性控制。 首先使用退化方法来精确地确定 神经元被癫痫发作活动不可逆地损伤。 细胞 最敏感的将被确定为将其位置， 传出投射 然后，采用免疫细胞化学方法 以确定可能被消耗的神经活性物质， 易受伤害的神经元和中间神经元的损伤。 由于已发现抑制作用的长期降低， 由于刺激诱发癫痫发作，细胞可能 将确定造成这一功能缺陷的原因。 他们 将以不涉及扣押的方式移走， 确定哪些中间神经元，当不可逆地受损时，可能是 负责癫痫发作后的变化。 很长的- 本研究的长期目标是描述 癫痫发作活动本身，并确定其机制， 癫痫发作会造成不可逆的损害。 这将允许 制定预防癫痫性脑损伤的策略， 延缓疾病可能的进展。

An experimental model has been developed to study the functional and structural consequences of seizure activity and to elucidate the normal structure and function of the hippocampus. Seizure activity in the hippocampus, which occurs in human temporal lobe epilepsy, the most common form of epilepsy, and in status epilepticus, a condition of continuous seizure discharge, is often associated with a characteristic pattern of hippocampal damage. This pattern of damage can be replicated in normal animals by electrical stimulation of the perforant path, the main afferent pathway to the hippocampus. Animals stimulated and allowed to recover for various periods can be used to determine the changes in function and structure that occur as a result of seizure activity. These animals therefore constitute a model of one aspect of the epileptic state, ie, the effects of repetitive seizures. Experiments have been designed to determine the relationship between selective neuron loss and the observed changes in both the excitability and inhibitory control of remaining neurons. Degeneration methods are used first to determine precisely which neurons are irreversibly damaged by seizure activity. The cells most sensitive will be identified as will the location of their efferent projections. Then, immunocytochemical methods are used to identify the neuroactive substances that may be depleted by the seizure-induced loss of susceptible neurons and interneurons. Since a long-lasting decrease in inhibition has been found to result from stimulation-induced seizures, the cells possibly responsible for this functional deficit will be identified. They will then be removed by means not involving seizures in order to determine which interneurons, when irreversibly damaged, might be responsible for the changes that occur after seizures. The long- term goals of this research are to describe the detrimental effects of seizure activity per se and to determine the mechanism by which seizures cause irreversible damage. This will allow the development of strategies to prevent epileptic brain damage and to retard the possibly progressive nature of the disorder.