Amygdala‐kindling induces a lasting reduction of GABA‐immunoreactive neurons in a discrete area of the ipsilateral piriform cortex
Amygdala‐kindling induces a lasting reduction of GABA‐immunoreactive neurons in a discrete area of the ipsilateral piriform cortex
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DOI：
10.1002/(sici)1098-2396(199808)29:4
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发表时间：
1998-08
期刊：
影响因子：
2.3
通讯作者：
H. Lehmann;U. Ebert;W. Löscher
中科院分区：
文献类型：
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作者：
H. Lehmann;U. Ebert;W. Löscher
多项证据表明，梨状皮层 (PC) 在颞叶癫痫点燃模型中发挥着关键作用，表明 PC 是癫痫网络的一部分，在点燃、促进和强化癫痫发作从杏仁核、海马或其他边缘脑区域向皮质和皮质下区域的扩散中起关键作用。杏仁核的点燃已被证明会引起同侧 PC 突触功效的持久变化，与癫痫灶中观察到的异常相当，但这些功能变化可能背后的神经化学变化尚不清楚。 PC 对点燃反应的兴奋性增强与 GABA 能神经传递的减少有关，这一可能性促使我们研究在大鼠基底外侧杏仁核 (BLA) 点燃后是否可以检测到 GABA 免疫反应性 PC 神经元的持续减少。此外，我们还测定了 BLA 中的 GABA 免疫反应性，以研究局灶组织中的 GABA 能神经元是否减少，正如之前在杏仁核激发大鼠中进行的神经化学和免疫细胞化学研究所表明的那样。使用三组年龄匹配的大鼠：（1）一组通过植入右侧 BLA 的双极电极进行电刺激而点燃的大鼠，（2）一组植入 BLA 但未受到刺激的大鼠，（3）一组未植入的初始对照大鼠。最后一次完全点燃癫痫发作后 40 天处死点燃的大鼠。另外两组大鼠与点燃的大鼠一起在同一天被处死，并且在整个免疫组织化学分析过程中同时处理来自点燃和对照大鼠的组织。 GABA 神经元被 GABA 单克隆抗体染色。 BLA 的点燃导致检查的所有切片水平的同侧和对侧 BLA 中 GABA 免疫反应神经元的数量显着减少。在 PC 中，对侧半球组间没有观察到显着差异，而在 BLA 电极同侧半球的前部和后部 PC 之间的过渡区观察到 GABA 免疫反应细胞显着减少。目前的发现增加了越来越多的证据表明 PC 在点燃诱发的癫痫发生中发挥着至关重要的作用。数据进一步证实，PC 不是一个均质结构，但该区域的前后轴在响应来自其他边缘脑区域的点燃刺激的神经化学（当然也是功能性）后果方面存在差异。突触 29:299–309, 1998。© 1998 Wiley-Liss, Inc.
Several lines of evidence indicate a critical role of the piriform cortex (PC) in the kindling model of temporal lobe epilepsy, suggesting that the PC is part of an epileptic network that is pivotal in the genesis of kindling, facilitating, and intensifying the spread of seizures from a focus in amygdala, hippocampus, or other limbic brain regions to cortical and subcortical regions. Kindling of the amygdala has been shown to induce long‐lasting changes in synaptic efficacy in the ipsilateral PC comparable to abnormalities seen in epileptic foci, but the neurochemical alterations possibly underlying these functional changes are not known. The possibility that the enhanced excitability of the PC in response to kindling is related to a reduction of GABAergic neurotransmission prompted us to examine if a lasting reduction in GABA‐immunoreactive PC neurons is detectable after kindling of the basolateral amygdala (BLA) in rats. Furthermore, GABA immunoreactivity was determined in the BLA in order to investigate whether GABAergic neurons decrease in focal tissue, as previously suggested by neurochemical and immunocytochemical studies in amygdala‐kindled rats. Three groups of age‐matched rats were used: (1) a group of rats that was kindled via electrical stimulation by a bipolar electrode implanted in the right BLA, (2) a group of BLA‐implanted but nonstimulated rats, and (3) a group of non‐implanted, naive control rats. The kindled rats were sacrificed 40 days after the last fully kindled seizure. The two other groups of rats were sacrificed together with the kindled rats on the same days, and tissues from kindled and control rats were treated concurrently throughout the immunohistochemical analysis. GABA neurons were stained by a monoclonal antibody to GABA. Kindling of the BLA led to a pronounced decrease in the number of GABA immunoreactive neurons in the ipsi‐ and contralateral BLA at all section levels examined. In the PC, no significant differences between groups were seen in the contralateral hemisphere, while a significant reduction in GABA immunoreactive cells was observed in the transition zone between anterior and posterior PC in the hemisphere ipsilateral to the BLA electrode. The present findings add to the accumulating evidence that the PC is critically involved in kindling‐induced epileptogenesis. The data furthermore substantiate that the PC is not a homogeneous structure but that there are differences along the anterior‐posterior axis of this region in neurochemical (and most certainly also functional) consequences in response to kindling stimulation from other limbic brain regions. Synapse 29:299–309, 1998. © 1998 Wiley‐Liss, Inc.