Audesirk G, Audesirk T
Neurotoxicology. 1983 Winter;4(4):13-26.
Although chronic exposure to lead has been correlated with a variety of behavioral and neurochemical deficits in humans and other mammals, little is known of the mechanisms of action of chronic lead at the level of the individual nerve cell. We have used the individually identifiable neurons of the freshwater pond snail Lymnaea stagnalis as a model system to investigate the effects of chronic low level (5 microM) lead exposure on neuronal physiology. Thirteen neuronal parameters were measured with intracellular microelectrode recording in each of six different identifiable neurons or homogeneous neuron clusters. Results were analyzed by a multivariate analysis of variance (MANOVA). MANOVA analysis indicates that there is a significant overall effect of lead exposure (p = 0.0001) and a significant interaction between lead and neuron type (p = 0.01). In most neuron types, chronic lead causes an increase in the resting potential, a slowing of recovery of the membrane potential after the undershoot of a spike, a decrease in spontaneous spiking activity, and a decrease in the input resistance. Lead also has differential effects on identifiable neurons, depressing excitability in some neuron types while not altering excitability in others.
尽管长期接触铅已被证明与人类和其他哺乳动物的多种行为及神经化学缺陷相关,但对于慢性铅在单个神经细胞水平上的作用机制却知之甚少。我们使用淡水池塘蜗牛椎实螺中可单独识别的神经元作为模型系统,来研究长期低水平(5微摩尔)铅暴露对神经元生理学的影响。通过细胞内微电极记录,在六个不同的可识别神经元或同质神经元簇中的每一个中测量了十三个神经元参数。结果通过多变量方差分析(MANOVA)进行分析。多变量方差分析表明,铅暴露存在显著的总体效应(p = 0.0001),并且铅与神经元类型之间存在显著的相互作用(p = 0.01)。在大多数神经元类型中,慢性铅会导致静息电位升高、峰电位下冲后膜电位恢复减慢、自发峰电位活动减少以及输入电阻降低。铅对可识别的神经元也有不同的影响,在某些神经元类型中抑制兴奋性,而在其他神经元类型中则不改变兴奋性。