Department of Pharmacology, Nihon University School of Dentistry, 1-8-13 Kanda-Surugadai, Chiyoda-ku, Tokyo 101-8310, Japan.
Neuroscience. 2010 Mar 10;166(1):341-53. doi: 10.1016/j.neuroscience.2009.12.023. Epub 2009 Dec 16.
Recent clinical studies have shown that the insular cortex (IC) is involved in temporal lobe epilepsy and suggested that the IC mediates spreading of epileptic activity from the temporal lobe, including the hippocampus and amygdala, to the frontal cortex. However, little is known about anatomical and physiological features of the IC in models of temporal lobe epilepsy. The present study evaluated the distribution pattern of GABAergic interneurons, especially parvalbumin (PV)- and somatostatin (SS)-immunopositive neurons, and excitatory propagation pattern in the IC of rats 4-7 days and 2 months after pilocarpine-induced status epilepticus (4-7 d and 2 m post-SE rats, respectively). The number of PV-immunopositive neuron profiles in the agranular IC (AI) significantly decreased by 24.6% and 41.5% in 7 d and 2 m post-SE rats, respectively. The dysgranular and granular IC (DI+GI) exhibited only 5.2% loss of PV-immunopositive neurons in 7 d post-SE rats, while 2 m post-SE rats showed 30.4% loss of PV-immunopositive neurons. There was no significant change of the SS-immunopositive neuron profile numbers in the AI and DI+GI of 7 d and 2 m post-SE rats. The regions with decreased numbers of PV-immunopositive neuron profiles overlapped with those where many degenerating cells were detected by Fluoro-Jade B staining. The area of excitatory propagation responding to electrical stimulation of the caudal AI was expanded in 4-7 d post-SE rats, and excitation frequently propagated to the frontal cortex including the motor cortex. Optical signals in the AI of 4-7 d post-SE rats were larger in amplitude than those of controls. In contrast to the AI, the DI of 4-7 d post-SE rats showed similar excitatory propagation pattern and amplitude to that of controls. These results suggest that the region-specific loss of PV-immunopositive neurons occurred in the AI 4-7 d after pilocarpine-induced status epilepticus, which may play an important role in facilitating excitatory propagation in the IC.
最近的临床研究表明，岛叶皮层（IC）参与颞叶癫痫，并提示 IC 介导癫痫活动从颞叶（包括海马体和杏仁核）向额叶皮层的扩散。然而，关于颞叶癫痫模型中 IC 的解剖学和生理学特征知之甚少。本研究评估了匹罗卡品诱导的癫痫持续状态（4-7 d 和 2 m 后 SE 大鼠）后 4-7 天和 2 个月大鼠 IC 中 GABA 能中间神经元，特别是副甲状腺球蛋白（PV）和生长抑素（SS）免疫阳性神经元的分布模式和兴奋性传播模式。在 7 d 和 2 m 后 SE 大鼠中，颗粒下 IC（AI）中 PV 免疫阳性神经元的数量分别显著减少了 24.6%和 41.5%。颗粒层和颗粒层 IC（DI+GI）在 7 d 后 SE 大鼠中仅失去 5.2%的 PV 免疫阳性神经元，而 2 m 后 SE 大鼠则失去 30.4%的 PV 免疫阳性神经元。在 7 d 和 2 m 后 SE 大鼠的 AI 和 DI+GI 中，SS 免疫阳性神经元的数量没有显著变化。PV 免疫阳性神经元数量减少的区域与用 Fluoro-Jade B 染色检测到大量变性细胞的区域重叠。对尾部 AI 电刺激反应的兴奋性传播区域在 4-7 d 后 SE 大鼠中扩大，并且兴奋经常传播到包括运动皮层在内的额叶皮层。4-7 d 后 SE 大鼠 AI 中的光信号幅度大于对照组。与 AI 相反，4-7 d 后 SE 大鼠的 DI 表现出与对照组相似的兴奋性传播模式和幅度。这些结果表明，在匹罗卡品诱导的癫痫持续状态后 4-7 天，AI 中出现了特定区域的 PV 免疫阳性神经元丢失，这可能在促进 IC 中的兴奋性传播中发挥重要作用。
