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首页> 外文期刊>The European Journal of Neuroscience >Extended secondhand tobacco smoke exposure induces plasticity in nucleus tractus solitarius second-order lung afferent neurons in young guinea pigs.
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Extended secondhand tobacco smoke exposure induces plasticity in nucleus tractus solitarius second-order lung afferent neurons in young guinea pigs.

机译：长时间暴露于二手烟中会导致豚鼠中的孤束核二级肺传入神经元发生可塑性。

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Infants and young children experiencing extended exposure to secondhand smoke (SHS) have an increased occurrence of asthma, as well as increased cough, wheeze, mucus production and airway hyper-reactivity. Plasticity in lung reflex pathways has been implicated in causing these symptoms, as have changes in substance P-related mechanisms. Using whole-cell voltage-clamp recordings and immunohistochemistry in brainstem slices containing anatomically identified second-order lung afferent nucleus tractus solitarius (NTS) neurons, we determined whether extended SHS exposure during the equivalent period of human childhood modified evoked or spontaneous excitatory synaptic transmission, and whether those modifications were altered by endogenous substance P. SHS exposure enhanced evoked synaptic transmission between sensory afferents and the NTS second-order neurons by eliminating synaptic depression of evoked excitatory postsynaptic currents (eEPSCs), an effect reversed by the neurokinin-1-receptor antagonist (SR140333). The recruitment of substance P in enhancing evoked synaptic transmission was further supported by an increased number of substance P-expressing lung afferent central terminals synapsing onto the second-order lung afferent neurons. SHS exposure did not change background spontaneous EPSCs. The data suggest that substance P in the NTS augments evoked synaptic transmission of lung sensory input following extended exposure to a pollutant. The mechanism may help to explain some of the exaggerated respiratory responses of children exposed to SHS.
机译：长时间接触二手烟（SHS）的婴幼儿患哮喘的发生率增加，并且咳嗽，喘息，粘液产生和气道反应过度也增加。肺反射通路的可塑性与这些物质P相关机制的改变有关，已引起这些症状。我们使用全细胞电压钳记录和免疫组织化学方法对脑干切片中含有解剖学鉴定的二阶肺传入神经孤核（NTS）神经元进行了研究，我们确定了在儿童期改良的诱发性或自发性兴奋性突触传递的等效时期，是否延长了SHS暴露时间，以及是否通过内源性物质P改变了这些修饰。SHS暴露通过消除诱发的兴奋性突触后突触电流（eEPSC）的突触抑制作用，增强了感觉传入和NTS二阶神经元之间的诱发突触传递，这种作用被神经激肽1受体逆转。拮抗剂（SR140333）。物质P在增强诱发的突触传递中的募集得到了更多数量的表达物质P的肺传入中枢末端突触到二级肺传入神经元的进一步支持。 SHS暴露不会改变背景自发EPSC。数据表明，长期暴露于污染物后，NTS中的P物质增强了肺感觉输入的诱发的突触传递。该机制可能有助于解释暴露于SHS的儿童的一些夸张的呼吸反应。

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