McCormick D A, Pape H C, Williamson A
Section of Neurobiology, Yale University School of Medicine, New Haven, CT.
Prog Brain Res. 1991;88:293-305. doi: 10.1016/s0079-6123(08)63817-0.
Norepinephrine (NE) has potent and long-lasting ionic effects on cortical and thalamic neurons. In cortical pyramidal cells, activation of beta-adrenergic receptors results in an enhanced excitability and responsiveness to depolarizing inputs. This enhanced excitability is expressed as a reduction in spike frequency adaptation and is mediated by a marked suppression of a slow Ca(++)-activated potassium current known as IAHP. In the thalamus, application of NE results in the suppression of ongoing rhythmic burst activity and a switch to the single spike firing mode of action potential generation. This effect is mediated through an alpha 1-adrenergic suppression of a resting leak potassium current, IKL, and through a beta-adrenoceptor-mediated enhancement of the hyperpolarization activated cation current Ih. Together with the actions of other neuromodulatory neurotransmitters (i.e., acetylcholine, histamine, serotonin) these effects facilitate the switch of these neurons from a state of rhythmic oscillation and low excitability during drowsiness and slow-wave sleep to a state of increased excitability and responsiveness during periods of waking, attentiveness and cognition.
去甲肾上腺素（NE）对皮质和丘脑神经元具有强大且持久的离子效应。在皮质锥体细胞中，β-肾上腺素能受体的激活会导致兴奋性增强以及对去极化输入的反应性增强。这种增强的兴奋性表现为动作电位频率适应性降低，并且是由一种称为IAHP的缓慢钙激活钾电流的显著抑制介导的。在丘脑中，应用NE会导致正在进行的节律性爆发活动受到抑制，并转变为动作电位产生的单峰发放模式。这种效应是通过α1-肾上腺素能受体对静息泄漏钾电流IKL的抑制以及β-肾上腺素能受体介导的超极化激活阳离子电流Ih的增强来介导的。与其他神经调节性神经递质（即乙酰胆碱、组胺、5-羟色胺）的作用一起，这些效应有助于这些神经元从困倦和慢波睡眠期间的节律性振荡和低兴奋性状态转变为清醒、注意力集中和认知期间的兴奋性和反应性增加的状态。
