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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Neonatal nicotine exposure alters hippocampal EEG and event-related potentials (ERPs) in rats.
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Neonatal nicotine exposure alters hippocampal EEG and event-related potentials (ERPs) in rats.

机译：新生儿尼古丁暴露会改变大鼠海马EEG和事件相关电位（ERP）。

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A consensus is forming that nicotine can damage the developing rat central nervous system. However, few studies have assessed the electrophysiological effects of neonatal nicotine exposure in rodents in brain regions known to be sensitive to the teratogenic properties of nicotine. In a previous study it was reported that 1.0 and 4.0 mg/kg/day nicotine exposure from postnatal days 4-9, a developmental period corresponding to human third-trimester exposure, significantly altered hippocampal event-related potentials (ERPs) but did not effect cortical ERPs, cortical EEG, or hippocampal EEG. Because alterations in behavior and cortical/hippocampal neurochemistry and morphology have been reported following nicotine exposure, the present study used a higher dose of nicotine during the postnatal period (6.0 mg/kg/day) determine if functional changes in the EEG of these regions might contribute to behavioral changes that have been observed. Male Sprague-Dawley rats were exposed to 6. 0 mg/kg/day nicotine via gastric infusion using an artificial rearing, "pup-in-the-cup," technique for 6 consecutive days (postnatal days 4-9). At adulthood, EEG and auditory ERPs were recorded from the cortex and hippocampus. There were no significant differences in EEG or ERPs recorded from the cortex between nicotine-treated and control subjects. Examination of the hippocampal EEG revealed significantly decreased power in the 1-2-Hz frequency band of nicotine-treated rats. In addition, there was a significantly attenuated P300 ERP response to a noise tone in the nicotine-treated rats compared to controls. These data indicate that neonatal nicotine exposure alters functional activity in the hippocampus of adult rats. These effects are likely to be the result of synaptic disorganization in the hippocampus, and indicate that neonatal nicotine exposure exerts teratogenic effects on the developing central nervous system, particularly the hippocampus, which persist into adulthood.
机译：尼古丁可以损害正在发育的大鼠中枢神经系统的共识正在形成。但是，很少有研究评估在已知对尼古丁的致畸性敏感的大脑区域的啮齿动物中新生儿尼古丁暴露的电生理作用。在先前的研究中，据报道，从出生后的第4-9天开始的1.0和4.0 mg / kg /天的尼古丁暴露，即对应于人类孕晚期的发育时期，显着改变了海马事件相关电位（ERP），但没有影响皮质ERP，皮质EEG或海马EEG。由于已经报道了尼古丁暴露后行为，皮质/海马神经化学和形态的改变，因此本研究在出生后使用更高剂量的尼古丁（6.0 mg / kg /天）来确定这些区域的脑电图功能改变是否可能有助于观察到的行为改变。雄性Sprague-Dawley大鼠连续6天（产后4-9天）通过人工饲养“杯中杯”技术通过胃浸液暴露于6. 0 mg / kg /天的尼古丁。在成年期，从皮质和海马体中记录了脑电图和听觉ERP。在尼古丁治疗组和对照组之间，从皮层记录的EEG或ERPs没有显着差异。对海马脑电图的检查显示，尼古丁治疗的大鼠的1-2-Hz频段功率显着降低。此外，与对照组相比，在尼古丁治疗的大鼠中，P300 ERP对噪声的反应明显减弱。这些数据表明，新生儿尼古丁暴露会改变成年大鼠海马的功能活动。这些作用可能是海马突触紊乱的结果，表明新生儿尼古丁暴露会对发育中的中枢神经系统，尤其是海马，持续到成年，产生致畸作用。

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