A longitudinal study of the effects of prenatal ethanol exposure on neuronal acquisition and death in the principal sensory nucleus of the trigeminal nerve: interaction with changes induced by transection of the infraorbital nerve

作     者：Miller, MW 

作者机构：Vet Affairs Med Ctr Res Serv Iowa City IA 52246 USA Univ Iowa Coll Med Dept Psychiat Iowa City IA 52242 USA Univ Iowa Coll Med Dept Pharmacol Iowa City IA 52242 USA 

出 版 物：《JOURNAL OF NEUROCYTOLOGY》 (脑细胞生物学杂志)

年 卷 期：1999年第28卷第12期

页      面：999-1015页

核心收录：

学科分类：0710[理学-生物学] 1001[医学-基础医学(可授医学、理学学位)] 07[理学] 071003[理学-生理学] 

基　　金：NIAAA NIH HHS [AA06916  AA09611  AA07568] Funding Source: Medline 

主　　题：年龄因素 轴突切断术 细胞计数 细胞死亡/药物作用 中枢神经系统抑制药/药理学 乙醇/药理学 纵向研究 上颌神经/细胞学 上颌神经/生理学 神经元 传入/细胞学 神经元 传入/药物作用 产前暴露迟发效应 大鼠 Sprague-Dawley 三叉神经核/细胞学 动物 女(雌)性 妊娠 大鼠 

摘      要：The present study determines (1) whether ethanol-induced microencephaly results from reductions in neuronal acquisition (i.e., cell proliferation and neuronal migration) and/or increases in neuronal death and (2) whether ethanol exacerbates death by the same mode as that for naturally occurring or lesion-induced neuronal death. Pregnant rats were exposed to a diet containing 6.7% (v/v) ethanol or an isocaloric control diet during the last two weeks of gestation. At birth, the right infraorbital nerves of the pups were transected. The numbers of neurons in the principal sensory nucleus of the trigeminal nerve (PSN) on both sides of the pons were examined at various prenatal and early postnatal timepoints. The numbers of pyknotic and argyrophilic PSN cells were also counted. Ethanol delayed and reduced (19.9%) the prenatal acquisition of PSN neurons. The postnatal decline in neuronal number (indicative of neuronal death) was significantly increased (10.6%) by ethanol. Likewise, the numbers of pyknotic and silver-stained cells were significantly higher in ethanol-treated rats. Lesion of the infraorbital nerve induced significant transsynaptic neuronal death in the control rats. Ethanol increased the amount of death caused by the lesion;however, it altered neither the timing of the neuronal loss nor the incidence of pyknosis or silver-staining. Therefore, ethanol affects both neuronal acquisition and survival;the greater effect being on neuronal acquisition. The timing and morphology of dying cells indicate that regardless of the cause (natural processes, ethanol-induced, or lesion-induced), neurons die in the developing PSN by the same mode.