Ciranna L, Licata F, Li Volsi G, Santangelo F
Instituto di Fisiologia Umana, Catania, Italy.
Brain Res. 1996 Dec 16;743(1-2):284-93. doi: 10.1016/s0006-8993(96)01057-8.
We have investigated the effects of noradrenaline (NA) on the spontaneous firing activity of red nucleus (RN) neurons recorded extracellularly in anesthetized rats by using an in vivo electrophysiological technique. Microiontophoretic applications of NA (5-100 nA for 30 s) modified the background firing rate in 99 out of 124 neurons and three different patterns of response were observed in distinct cells. In 61% of the responding neurons NA decreased the mean firing rate, whereas 22% of the neurons responded to NA application with an increase of their spiking activity; in a smaller group of cells (17%) NA exerted a biphasic inhibitory/excitatory effect on the spontaneous firing rate. The effects of NA were reversible and dose-dependent. From histological examination, the neurons responding to NA with a purely inhibitory effect were scattered throughout the RN. On the other hand, the neurons responding to NA with an excitation were found to be more numerous in the dorso-medial part of the RN, whereas the neurons in which NA induced biphasic effects appeared to be segregated in the outer lateral portion of the RN. The alpha 2-adrenoceptor antagonist yohimbine completely blocked the inhibitory effect of NA but was unable to antagonize the excitatory response. In addition, the inhibitory effect of NA was mimicked by clonidine, a selective agonist of alpha 2-adrenoceptors; clonidine had no effect on those cells which responded to NA with an increase of the mean firing rate. The excitatory effect of NA was mimicked by the beta-receptor agonist isoprenaline and was antagonized by timolol, a selective antagonist of beta-adrenoceptors. Isoprenaline was ineffective in those cells in which NA exerted inhibitory responses. Taken together, our results indicate that the inhibitory effect of NA on the firing activity of rat RN neurons were mediated by alpha 2-adrenoceptors, whereas beta-adrenoceptors were responsible for the excitatory effects.
我们采用体内电生理技术，研究了去甲肾上腺素（NA）对麻醉大鼠红核（RN）神经元细胞外记录的自发放电活动的影响。通过微离子电泳施加NA（5 - 100 nA，持续30 s），改变了124个神经元中99个神经元的背景放电率，并且在不同细胞中观察到三种不同的反应模式。在61%的反应神经元中，NA降低了平均放电率，而22%的神经元对NA施加的反应是其放电活动增加；在一小部分细胞（17%）中，NA对自发放电率产生双相抑制/兴奋作用。NA的作用是可逆的且呈剂量依赖性。组织学检查表明，对NA产生纯抑制作用的神经元散布于整个红核。另一方面，对NA产生兴奋反应的神经元在红核的背内侧部分较多，而NA诱导双相作用的神经元似乎分隔在红核的外侧部分。α2 - 肾上腺素能受体拮抗剂育亨宾完全阻断了NA的抑制作用，但无法拮抗兴奋反应。此外，NA的抑制作用可被α2 - 肾上腺素能受体的选择性激动剂可乐定模拟；可乐定对那些对NA反应为平均放电率增加的细胞没有影响。NA的兴奋作用可被β - 受体激动剂异丙肾上腺素模拟，并被β - 肾上腺素能受体的选择性拮抗剂噻吗洛尔拮抗。异丙肾上腺素对NA产生抑制反应的细胞无效。综上所述，我们的结果表明，NA对大鼠红核神经元放电活动的抑制作用由α2 - 肾上腺素能受体介导，而β - 肾上腺素能受体则负责兴奋作用。
