Acute nicotine exposure and modulation of a spinal motor circuit in embryonic zebrafish.
Acute nicotine exposure and modulation of a spinal motor circuit in embryonic zebrafish.
复制标题
胚胎斑马鱼的急性尼古丁暴露和脊髓运动回路的调节。
DOI：
10.1016/j.taap.2008.08.023
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发表时间：
2009
影响因子：
3.8
通讯作者：
Svoboda,KurtR
中科院分区：
文献类型：
--
作者：
Thomas,LatoyaT;Welsh,Lillian;Galvez,Fernando;Svoboda,KurtR
斑马鱼模型系统是研究神经系统发育的理想系统。最终，人们希望将发育生物学与行为的各个方面联系起来。我们正在研究尼古丁暴露对斑马鱼神经系统发育的影响，并且以前已经表明长期尼古丁暴露会导致瘫痪。我们还观察到胚胎在暴露的最初几分钟随着肌肉组织弯曲率的增加而移动。这种尼古丁诱导的行为表现为脊髓肌肉组织弯曲率的增加，其自发地在受精后18 h开始。行为观察促使系统表征尼古丁诱导的调制斑马鱼胚胎运动输出;弯曲的躯干肌肉组织。我们首先在有和没有绒毛膜的斑马鱼胚胎中表征胚胎运动输出。然后，我们描述了在28 °C和25 °C下培养的胚胎的运动输出。沿着温度变化的脱氯作用影响胚胎弯曲率。我们发现，尼古丁暴露增加胚胎运动输出。尼古丁暴露导致肌肉组织弯曲，以左-右-左的方式交替。尼古丁能够在缺乏脊髓上输入的胚胎中产生这种表型。然后，我们表征了尼古丁流入和流出的动力学，并证明低至1 μM的尼古丁可以破坏胚胎生理学。两者合计，这些结果表明，存在烟碱乙酰胆碱受体（nAChRs）与胚胎脊髓运动电路在胚胎发育早期。
The zebrafish model system is ideal for studying nervous system development. Ultimately, one would like to link the developmental biology to various aspects of behavior. We are studying the consequences of nicotine exposure on nervous system development in zebrafish and have previously shown that chronic nicotine exposure produces paralysis. We also have made observations that the embryos moved in the initial minutes of the exposure as the bend rates of the musculature increased. This nicotine induced behavior manifests as an increase in the rate of spinal musculature bends, which spontaneously begin at ∼18 h post fertilization. The behavioral observations prompted the systematic characterization of nicotine-induced modulation of zebrafish embryonic motor output; bends of the trunk musculature. We first characterized embryonic motor output in zebrafish embryos with and without their chorions. We then characterized the motor output in embryos raised at 28 °C and 25 °C. The act of dechorionation along with temperature influenced the embryonic bend rate. We show that nicotine exposure increases embryonic motor output. Nicotine exposure caused the musculature bends to alternate in a left–right–left fashion. Nicotine was able to produce this phenotype in embryos lacking supraspinal input. We then characterize the kinetics of nicotine influx and efflux and demonstrate that nicotine as low as 1 μM can disrupt embryonic physiology. Taken together, these results indicate the presence of nicotinic acetylcholine receptors (nAChRs) associated with embryonic spinal motor circuits early in embryogenesis.