乙醇诱导的行为和神经生理嗅觉反应增强的胎儿期发生过程。
Ontogeny of the enhanced fetal-ethanol-induced behavioral and neurophysiologic olfactory response to ethanol odor.
机构信息
Department of Neuroscience and Physiology, State University of New York, Upstate Medical University, Syracuse, New York, USA.
出版信息
Alcohol Clin Exp Res. 2010 Feb;34(2):206-13. doi: 10.1111/j.1530-0277.2009.01083.x. Epub 2009 Nov 24.
BACKGROUND
Studies report a fundamental relationship between chemosensory function and the responsiveness to ethanol, its component orosensory qualities, and its odor as a consequence of fetal ethanol exposure. Regarding odor, fetal exposed rats display enhanced olfactory neural and behavioral responses to ethanol odor at postnatal (P) day 15. Although these consequences are absent in adults (P90), the behavioral effect has been shown to persist into adolescence (P37). Given the developmental timing of these observations, we explored the decay in the response to ethanol odor by examining ages between P37 and young adulthood. Moreover, we sought to determine whether the P15 neurophysiologic effect persists, at least, to P40.
METHODS
Behavioral and olfactory epithelial (OE) responses of fetal ethanol exposed and control rats were tested at P40, P50, P60, or P70. Whole-body plethysmography was used to quantify each animal's innate behavioral response to ethanol odor. We then mapped the odorant-induced activity across the OE in response to different odorants, including ethanol, using optical recording methods.
RESULTS
Relative to controls, ethanol exposed animals showed an enhanced behavioral response to ethanol odor that, while significant at each age, decreased in magnitude. These results, in conjunction with previous findings, permitted the development of an ontologic odor response model of fetal exposure. The fitted model exemplifies that odor-mediated effects exist at birth, peak in adolescence and then decline, becoming absent by P90. There was no evidence of an effect on the odor response of the OE at any age tested.
CONCLUSIONS
Fetal exposure yields an enhanced behavioral response to ethanol odor that peaks in adolescence and wanes through young adulthood. This occurs absent an enhanced response of the OE. This latter finding suggests that by P40 the OE returns to an ethanol "neutral" status and that central mechanisms, such as ethanol-induced alterations in olfactory bulb circuitry, underlie the enhanced behavioral response. Our study provides a more comprehensive understanding of the ontogeny of fetal-ethanol-induced olfactory functional plasticity and the behavioral response to ethanol odor.
背景
研究报告表明，化学感觉功能与对乙醇及其成分味觉品质的反应以及胎儿乙醇暴露后乙醇气味的嗅觉之间存在基本关系。关于气味，暴露于乙醇的胎儿大鼠在出生后第 15 天（P）显示出对乙醇气味的嗅觉神经和行为反应增强。尽管这些后果在成年期（P90）不存在，但已经表明行为效应持续到青春期（P37）。鉴于这些观察结果的发展时间，我们通过检查 P37 与成年早期之间的年龄来探索对乙醇气味的反应消退。此外，我们试图确定至少到 P40 时，P15 的神经生理效应是否仍然存在。
方法
测试了胎儿乙醇暴露和对照大鼠在 P40、P50、P60 或 P70 时的行为和嗅觉上皮（OE）反应。全身 plethysmography 用于量化每个动物对乙醇气味的先天行为反应。然后，我们使用光学记录方法在 OE 上绘制对不同气味（包括乙醇）的气味诱导活性图。
结果
与对照组相比，暴露于乙醇的动物对乙醇气味的行为反应增强，尽管在每个年龄段都有显著差异，但强度降低。这些结果与之前的发现相结合，允许开发胎儿暴露的本体气味反应模型。拟合模型举例说明了出生时存在气味介导的影响，在青春期达到高峰，然后下降，到 P90 时消失。在测试的任何年龄都没有证据表明 OE 的气味反应受到影响。
结论
胎儿暴露导致对乙醇气味的行为反应增强，在青春期达到高峰，并在青年期减弱。这发生在 OE 反应增强的情况下。后一种发现表明，到 P40 时，OE 恢复到乙醇“中性”状态，并且中枢机制，例如嗅球电路中乙醇诱导的改变，是增强的行为反应的基础。我们的研究提供了对胎儿乙醇诱导嗅觉功能可塑性和对乙醇气味的行为反应的发育过程的更全面理解。
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