ACTIONS OF NORADRENALINE RECORDED INTRACELLULARLY IN RAT HIPPOCAMPAL CA1 PYRAMIDAL NEURONS, INVITRO
ACTIONS OF NORADRENALINE RECORDED INTRACELLULARLY IN RAT HIPPOCAMPAL CA1 PYRAMIDAL NEURONS, INVITRO
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DOI：
10.1113/jphysiol.1986.sp016006
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发表时间：
1986-03-01
影响因子：
5.5
通讯作者：
NICOLL, RA
中科院分区：
文献类型：
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作者：
MADISON, DV;NICOLL, RA
使用标准细胞内和单电极电压钳记录技术在大鼠体外海马切片中研究 CA1 锥体神经元，以检查去甲肾上腺素 (NA) 的作用。 NA 对锥体神经元的静息膜电位有两种不同的影响：要么是超极化伴随着膜输入电阻的降低，要么是不太常见的去极化伴随着输入电阻的增加。在许多细胞中，观察到超极化和去极化这两种效应。去极化是由去甲肾上腺素能β-受体介导的。超极化更难以表征，但可能是由α-受体激活引起的。 NA 降低了去极化诱导动作电位后缓慢的钙激活钾后超极化 (a.h.p.) 的幅度和持续时间。 NA的这种作用是由β1-去甲肾上腺素能受体介导的。 NA，在河豚毒素和四乙铵存在的情况下，降低了 a.h.p。而不降低之前的钙动作电位的大小。这与钙通道阻滞剂镉的作用不同，镉会降低钙动作电位和 a.h.p。并联。此外，在阻断钾电流后，NA 不会降低在电压钳下记录的钙或钡电流的幅度。这种钙激活 a.h.p 阻断的功能性结果。动作电位放电的调节减少，从而增强神经元对去极化刺激（例如谷氨酸应用或通过记录电极的电流）的兴奋反应。我们得出的结论是，NA 对钙激活钾电导和静息膜电位的影响可以相互作用，从而增加海马锥体神经元反应性的信噪比。
CA1 pyramidal neurones were studied in rat in vitro hippocampal slices using standard intracellular and single-electrode voltage-clamp recording techniques to examine the actions of noradrenaline (NA). NA had two different effects on the resting membrane potential of pyramidal neurones; either a hyperpolarization accompanied by a decrease in membrane input resistance, or less commonly, a depolarization accompanied by an increase in input resistance. In many cells, both effects, a hyperpolarization followed by a depolarization were observed. The depolarization was mediated by a noradrenergic .beta.-receptor. The hyperpolarization was more difficult to characterize, but may result from .alpha.-receptor activation. NA reduced the amplitude and duration of the slow calcium-activated potassium after-hyperpolarization (a.h.p.) that follows depolarization-induced action potentials. This action of NA was mediated by .beta.1-noradrenergic receptors. NA, in the presence of tetrodotoxin and tetraethylammonium, reduced the a.h.p. without reducing the size of the calcium action potential which preceded it. This was unlike the action of the calcium channel blocker, cadmium, which reduced the calcium action potential and the a.h.p. in parallel. Furthermore, NA did not reduce the amplitude of calcium or barium currents recorded under voltage clamp after blockade of potassium currents. A functional consequence of this blockade of the calcium-activated a.h.p. was a reduction of the accommodation of action potential discharge such that the excitatory responses of the neurone to depolarizing stimuli, such as glutamate application or current passed through the recording electrode, were enhanced. We conclude that the effects of NA on calcium-activated potassium conductance and on resting membrane potential can interact to increase the signal-to-noise ratio of hippocampal pyramidal neurone responsiveness.