Chae H J, Kang J S, Cho S B, Jin B G, Won S J, Gwag B J, Kim H R
Department of Dental Pharmacology, Wonkwang University School of Dentistry, Iksan, Chonbuk, S. Korea.
Res Commun Mol Pathol Pharmacol. 1999;104(1):31-41.
Both direct and indirect environmental stress to the brain can increase the expression of transcription factor c-fos in various populations of neurons. In this study, we examined whether the intraperitoneal injections of lidocaine at doses inducing convulsions within 10 min, increased the level of c-fos mRNA and protein in forebrain areas. In in situ hybridization using [35S]UTP-labeled antisense c-fos, cRNA increased c-fos mRNA levels through the hippocampal formation, piriform cortex, septum, caudate-putamen, neostriatum, and amygdala within 2 hr. In parallel with the mRNA expression, c-fos protein immuno-reactivity was also observed in the same forebrain areas. In contrast to the seizure activity and wide-spread neuronal degeneration following kainate treatment, injections of lidocaine did not produce neuronal death within three days. The present study indicates that lidocaine induces convulsions and c-fos expression without causing neurotoxicity.
大脑所遭受的直接和间接环境压力均可增加各种神经元群体中转录因子c-fos的表达。在本研究中，我们检测了腹腔注射在10分钟内诱导惊厥的剂量的利多卡因，是否会增加前脑区域中c-fos mRNA和蛋白质的水平。在使用[35S]UTP标记的反义c-fos进行的原位杂交中，cRNA在2小时内通过海马结构、梨状皮质、隔区、尾状核-壳核、新纹状体和杏仁核增加了c-fos mRNA水平。与mRNA表达平行，在相同的前脑区域也观察到了c-fos蛋白免疫反应性。与海藻酸处理后的癫痫活动和广泛的神经元变性相反，注射利多卡因在三天内未导致神经元死亡。本研究表明，利多卡因可诱导惊厥和c-fos表达而不引起神经毒性。
