Chernigovskaya Elena V, Dorofeeva Nadezhda A, Nasluzova Elizaveta V, Kulikov Alexey A, Ovsyannikova Victoria V, Glazova Margarita V
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 Thorez pr., 194223 St. Petersburg, Russia.
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, 44 Thorez pr., 194223 St. Petersburg, Russia.
Epilepsy Behav. 2018 Nov;88:227-234. doi: 10.1016/j.yebeh.2018.09.023. Epub 2018 Oct 11.
It is known that audiogenic seizure (AGS) expression is based on the activation of the midbrain structures such as the inferior colliculus (IC). It was demonstrated that excessive sound exposure during the postnatal developments of the IC in rats led to AGS susceptibility in adulthood, which correlated with underdevelopment of the IC. In adult rodents, noise overstimulation induced apoptosis in the IC. The purpose of this study was to investigate postnatal development of the IC in rats genetically prone to AGS and to check if audiogenic kindling would activate apoptosis and/or proliferation in the IC. In our study, we used inbred audiogenic Krushinsky-Molodkina (KM) rats, which are characterized by age-dependent seizure expression. Analysis of postnatal development showed the increased number of proliferating cells in the IC central nucleus of KM rats on the 14th postnatal day (P14) in comparison with those of Wistar rats. Moreover, we also observed increased apoptosis level and decreased general cell population in the IC central nucleus. These data pointed towards a delayed development of the IC in KM rats. Analysis of the IC central nucleus of KM rat after audiogenic kindling for a week, with one AGS per day, demonstrated dramatically increased cell death, which was accompanied with a reduction of general cell population. Audiogenic kindling also decreased proliferation in the IC central nucleus. However, a week after the last AGS, the number of proliferating cells was increased, which supposes a certain compensatory mechanism to prevent cell loss.
已知听源性癫痫发作(AGS)的表现基于中脑结构如下丘(IC)的激活。已证明,大鼠IC在出生后发育期间过度暴露于声音会导致成年期对AGS易感,这与IC发育不全相关。在成年啮齿动物中,噪声过度刺激会诱导IC中的细胞凋亡。本研究的目的是调查易患AGS的大鼠IC的出生后发育情况,并检查听源性点燃是否会激活IC中的细胞凋亡和/或增殖。在我们的研究中,我们使用了近交系听源性克鲁申斯基-莫洛迪纳(KM)大鼠,其特征是癫痫发作表现具有年龄依赖性。出生后发育分析显示,与Wistar大鼠相比,KM大鼠出生后第14天(P14)IC中央核中增殖细胞数量增加。此外,我们还观察到IC中央核中细胞凋亡水平升高,总体细胞数量减少。这些数据表明KM大鼠IC发育延迟。对每天进行一次AGS、听源性点燃一周后的KM大鼠IC中央核进行分析,结果显示细胞死亡显著增加,同时总体细胞数量减少。听源性点燃还降低了IC中央核中的增殖。然而,在最后一次AGS后一周,增殖细胞数量增加,这推测存在某种补偿机制以防止细胞损失。