Silveira D C, Schachter S C, Schomer D L, Holmes G L
Department of Neurology, Beth Israel Deaconess Medical Center, Kirstein 478 and Harvard Medical School, Boston, MA 02115, USA.
Epilepsy Res. 2000 Mar;39(1):1-12. doi: 10.1016/s0920-1211(99)00106-0.
Autonomic changes accompany seizures in both animals and humans. While ictal autonomic dysfunction can be life-threatening, the participating neural networks involved are poorly understood. In this study we examined the activation of Fos following generalized seizures in brainstem structures known to mediate autonomic function. Adult female rats were sacrificed 2 h after flurothyl-induced seizures. Double-immunostaining for c-Fos and dopamine-beta-hydroxylase (DBH), and c-Fos and phenylethanol-N-methyl-transferase (PNMT) were performed in brainstem slices. Numbers of DBH-labeled neurons expressing Fos-like immunoreactivity (FLI) (DBH/Fos) and PNMT labeled neurons expressing FLI (PNMT/Fos) were counted in the noradrenergic (A1, A2, A5, A7) and adrenergic (C1, C2) cell groups localized in pons and medulla oblongata. Among the experimental animals, the highest degree of co-localization of DBH/Fos neurons was observed in the locus coeruleus (A6; 87.7%), and in the A1(72.8%) cell group located in the caudal ventrolateral medulla (VLM). No co-localization of DBH/Fos neurons was observed in control animals. The highest degree of co-localization of PNMT/Fos neurons was observed in the C1 adrenergic cell group (84.2%) located in the rostral VLM. Control animals showed very few (5.5%) PNMT/Fos co-localized neurons in the C1 adrenergic cell group. Our results indicate that flurothyl-induced generalized seizures in rats activate catecholaminergic neurons in the pons and medulla oblongata. Further studies are necessary to determine whether activation of brainstem catecholaminergic neurons contribute to the autonomic manifestations that frequently accompany epileptic seizures.
在动物和人类中，癫痫发作都会伴随自主神经变化。虽然发作期自主神经功能障碍可能危及生命，但其中涉及的参与神经网络却知之甚少。在本研究中，我们检测了已知介导自主神经功能的脑干结构在全身性癫痫发作后Fos的激活情况。成年雌性大鼠在氟烷诱发癫痫发作后2小时被处死。在脑干切片中进行c-Fos与多巴胺-β-羟化酶（DBH）以及c-Fos与苯乙醇-N-甲基转移酶（PNMT）的双重免疫染色。对位于脑桥和延髓的去甲肾上腺素能（A1、A2、A5、A7）和肾上腺素能（C1、C2）细胞群中表达Fos样免疫反应性（FLI）的DBH标记神经元（DBH/Fos）和表达FLI的PNMT标记神经元（PNMT/Fos）进行计数。在实验动物中，DBH/Fos神经元共定位程度最高的是在蓝斑（A6；87.7%）以及位于尾侧腹外侧延髓（VLM）的A1细胞群（72.8%）。在对照动物中未观察到DBH/Fos神经元的共定位。PNMT/Fos神经元共定位程度最高的是在位于头侧VLM的C1肾上腺素能细胞群（84.2%）。对照动物在C1肾上腺素能细胞群中显示出极少（5.5%）的PNMT/Fos共定位神经元。我们的结果表明，氟烷诱发的大鼠全身性癫痫发作激活了脑桥和延髓中的儿茶酚胺能神经元。有必要进一步研究以确定脑干儿茶酚胺能神经元的激活是否导致癫痫发作时频繁出现的自主神经表现。
