Pereno Germán L, Balaszczuk Verónica, Beltramino Carlos A
Cátedra de Neurofisiología y Psicofisiología, Facultad de Psicología, Universidad Nacional de Córdoba 5000, Córdoba, Argentina.
Exp Toxicol Pathol. 2011 Mar;63(3):291-9. doi: 10.1016/j.etp.2010.02.001. Epub 2010 Feb 24.
The medial extended amygdala modulates pheromonal perception, influencing emotional and social behavior. As the amygdala is part of neuronal circuits that are very sensitive to excitability, its neurons are targets of seizures in temporal lobe epilepsy. It has been suggested that the hippocampus is strongly involved this pathology. There is less consistent information, however, on the effects of this disease in the amygdala. The effects of status epilepticus on the medial extended amygdala were analyzed by immunohistochemistry for neural stress and by the amino-cupric-silver technique for neuronal death in rats after kainic acid (KA) administration. Sixty adult Wistar male rats were used. Thirty animals received an injection of KA, and 30 were injected with saline. After 2, 4, 12, 24 and 48 h survival the brains were stained for Fos and FosB and for neuronal death. In the present study we show that KA induces Fos and FosB expression in neurons of the medial extended amygdala after 2, 4-48 h, with time courses that are different between them and from control animals. While Fos-IR peaks at 2-4 h post KA and then decreases, FosB-IR increases in the same period reaching its highest expression at 24-48 h. Moreover, KA injection produced massive neuronal death with a peak at 24 h. This neurodegeneration paralleled FosB-IR protein expression. These findings show that KA produces neuronal stress and activation of early genes and neuronal death in the medial extended amygdala, demonstrating the vulnerability of its neurons to the epileptogenic effects of KA.
内侧扩展杏仁核调节信息素感知，影响情绪和社会行为。由于杏仁核是对兴奋性非常敏感的神经回路的一部分，其神经元是颞叶癫痫发作的靶点。有人提出海马体与这种病理密切相关。然而，关于这种疾病对杏仁核的影响，信息并不一致。通过免疫组织化学检测神经应激以及用氨基铜银技术检测给予 kainic acid（KA）后大鼠神经元死亡情况，分析癫痫持续状态对内侧扩展杏仁核的影响。使用了 60 只成年雄性 Wistar 大鼠。30 只动物注射 KA，30 只注射生理盐水。在存活 2、4、12、24 和 48 小时后，对大脑进行 Fos 和 FosB 染色以及神经元死亡检测。在本研究中，我们表明 KA 在 2、4 - 48 小时后诱导内侧扩展杏仁核神经元中 Fos 和 FosB 的表达，它们之间以及与对照动物的时间进程不同。虽然 Fos 免疫反应性在 KA 注射后 2 - 4 小时达到峰值，然后下降，但 FosB 免疫反应性在同一时期增加，在 24 - 48 小时达到最高表达。此外，KA 注射导致大量神经元死亡，在 24 小时达到峰值。这种神经退行性变与 FosB 免疫反应性蛋白表达平行。这些发现表明 KA 在内侧扩展杏仁核中产生神经元应激、早期基因激活和神经元死亡，证明其神经元对 KA 的致痫作用具有易损性。
