Nicotinic control of axon excitability regulates thalamocortical transmission
Nicotinic control of axon excitability regulates thalamocortical transmission
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DOI：
10.1038/nn1956
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发表时间：
2007-09-01
影响因子：
25
通讯作者：
Metherate, Raju
中科院分区：
文献类型：
--
作者：
Kawai, Hideki;Lazar, Ronit;Metherate, Raju
丘脑皮质通路是由丘脑中继神经元产生的一束有髓轴突，将感觉信息传递到新皮质。由于轴突激发是信息从丘脑到皮质传递的必要步骤，因此它代表了潜在的控制点。我们现在表明，在成年小鼠中，听觉丘脑皮质通路初始部分烟碱乙酰胆碱受体（nAChR）的激活通过调节轴突兴奋性来调节丘脑皮质信息传递。外源性尼古丁增强了体外丘脑皮质轴突诱发动作电位放电的概率和同步性，但对突触释放机制影响不大。在体内，丘脑皮质通路中 nAChR 的阻断减少了声音诱发的皮质反应，尤其是由接近声学阈值的声音诱发的反应。这些数据表明，内源性乙酰胆碱激活丘脑皮质通路中的 nAChR，以降低丘脑皮质传递的阈值并增加感觉诱发的皮质反应的强度。我们的结果表明，神经递质可以通过调节沿有髓鞘丘脑皮质轴突的传导来调节感觉处理。
The thalamocortical pathway, a bundle of myelinated axons that arises from thalamic relay neurons, carries sensory information to the neocortex. Because axon excitation is an obligatory step in the relay of information from the thalamus to the cortex, it represents a potential point of control. We now show that, in adult mice, the activation of nicotinic acetylcholine receptors ( nAChRs) in the initial portion of the auditory thalamocortical pathway modulates thalamocortical transmission of information by regulating axon excitability. Exogenous nicotine enhanced the probability and synchrony of evoked action potential discharges along thalamocortical axons in vitro, but had little effect on synaptic release mechanisms. In vivo, the blockade of nAChRs in the thalamocortical pathway reduced sound-evoked cortical responses, especially those evoked by sounds near the acoustic threshold. These data indicate that endogenous acetylcholine activates nAChRs in the thalamocortical pathway to lower the threshold for thalamocortical transmission and to increase the magnitude of sensory-evoked cortical responses. Our results show that a neurotransmitter can modulate sensory processing by regulating conduction along myelinated thalamocortical axons.