Elam M, Yao T, Svensson T H, Thoren P
Brain Res. 1984 Jan 9;290(2):281-7. doi: 10.1016/0006-8993(84)90945-4.
The brain norepinephrine (NE) neurons in the nucleus locus coeruleus (LC) have been claimed to be involved both in the regulation of behavioral functions, e.g. vigilance and arousal reactions, and in cardiovascular control. Recent studies from this laboratory have also shown that cardiovascular, vagal afferents can participate in the regulation of the LC neurons in the rat. Utilizing electrophysiological techniques, we have now studied the effects of activation of blood volume receptors or arterial baroreceptors on the firing rate of single cells in the LC and, parallelly, on splanchnic, sympathetic discharge in the chloral hydrate anesthetized rat. Blood volume load (0.5-5 ml heparinized blood, intravenously administered) induced a reduction in both LC neuronal firing rate and splanchnic nerve activity (SNA), effects which were readily and completely reversed by withdrawal of the corresponding amount of blood. In comparison, the central LC neurons were more sensitive to blood volume expansion than the peripheral splanchnic nerves. The effects of blood volume load on LC and SNA remained unaffected after deafferention of arterial baroreceptors. Blood pressure elevation, induced by slow intravenous infusion of NE or angiotensin (AII) (total dose 2 micrograms/kg), caused an immediate reduction in both the firing rate of most of the LC cells tested as well as in SNA. While the effect on SNA was abolished by deafferentation of arterial baroreceptors, the effect on central LC activity remained largely unaffected. Consequently, these data strengthen the concept that brain NE neurons in the LC are subject to control by peripheral blood volume receptors, analogously to peripheral sympathetic nerves. Arterial baroreceptors may still participate in the control of central noradrenergic nerve activity, but in contrast to their function for SNA they are not critical for the inhibition of LC neurons by blood pressure elevation. Rather, these two cardiovascular afferent systems may participate in the physiological regulation of the LC activity in a complimentary and convergent fashion.
蓝斑核(LC)中的脑去甲肾上腺素(NE)神经元被认为既参与行为功能的调节,如警觉和觉醒反应,也参与心血管控制。本实验室最近的研究还表明,心血管迷走传入神经可以参与大鼠LC神经元的调节。利用电生理技术,我们现在研究了血容量受体或动脉压力感受器激活对LC中单个细胞放电率的影响,同时也研究了对水合氯醛麻醉大鼠内脏交感神经放电的影响。血容量负荷(静脉注射0.5 - 5 ml肝素化血液)导致LC神经元放电率和内脏神经活动(SNA)均降低,通过抽取相应量的血液,这些影响很容易且完全逆转。相比之下,中枢LC神经元对血容量扩张比外周内脏神经更敏感。在去除动脉压力感受器传入神经后,血容量负荷对LC和SNA的影响仍然不受影响。通过缓慢静脉注射NE或血管紧张素(AII)(总剂量2微克/千克)诱导血压升高,导致大多数受试LC细胞的放电率以及SNA立即降低。虽然动脉压力感受器传入神经去除后对SNA的影响被消除,但对中枢LC活动的影响在很大程度上仍然不受影响。因此,这些数据强化了这样一种概念,即LC中的脑NE神经元类似于外周交感神经,受到外周血容量受体的控制。动脉压力感受器可能仍然参与中枢去甲肾上腺素能神经活动的控制,但与它们对SNA的功能相反,它们对血压升高抑制LC神经元并不关键。相反,这两个心血管传入系统可能以互补和汇聚的方式参与LC活动的生理调节。