Susan Samueli Center for Integrative Medicine, Department of Medicine, School of Medicine, University of California, Irvine, Irvine, California 92697-4075, USA.
Am J Physiol Regul Integr Comp Physiol. 2010 Nov;299(5):R1369-76. doi: 10.1152/ajpregu.00361.2010. Epub 2010 Aug 18.
We have shown that electroacupuncture (EA) inhibits sympathoexcitatory rostral ventrolateral medulla (rVLM) neurons and reflex responses following activation of a long-loop pathway in the arcuate nucleus and ventrolateral periaqueductal gray (vlPAG). Additionally, EA at P 5-6 acupoints (overlying the median nerve) activates serotonin-containing neurons in the nucleus raphé pallidus (NRP), which, in turn, inhibit rVLM neurons. Although direct projections from the vlPAG to the rVLM exist, it is uncertain whether an indirect pathway through the NRP serves an important role in vlPAG-rVLM cardiovascular modulation. Therefore, the splanchnic nerve (SN) was stimulated to induce cardiovascular sympathoexcitatory reflexes, and EA was applied at P 5-6 acupoints in α-chloralose-anesthetized cats. A single-barreled recording electrode was inserted into the NRP or rVLM. Microinjection of DL-homocysteic acid (DLH) into the vlPAG increased the NRP neuronal response to SN stimulation (5 ± 1 to 12 ± 2 spikes/30 stim). Likewise, EA at P 5-6 for 30 min increased the NRP response to SN stimulation (3 ± 1 to 10 ± 2 spikes/30 stim), an effect that could be blocked by microinjection of kynurenic acid (KYN) into the caudal vlPAG. Furthermore, the reflex increase in blood pressure induced by application of bradykinin to the gallbladder and the rVLM cardiovascular presympathetic neuronal response to SN stimulation was inhibited by injection of DLH into the vlPAG, a response that was reversed by injection of KYN into the NRP. These results indicate that EA activates the vlPAG, which excites the NRP to, in turn, inhibit rVLM presympathetic neurons and reflex cardiovascular sympathoexcitatory responses.
我们已经证明,电针(EA)抑制交感兴奋性延髓头端腹外侧区(rVLM)神经元和弓状核及腹外侧导水管周围灰质(vlPAG)长环通路激活后的反射反应。此外,针刺 P5-6 穴位(正中神经上方)可激活中缝苍白核(NRP)中含 5-羟色胺的神经元,进而抑制 rVLM 神经元。虽然 vlPAG 与 rVLM 之间存在直接投射,但通过 NRP 的间接通路是否在 vlPAG-rVLM 心血管调节中发挥重要作用尚不确定。因此,刺激内脏神经(SN)以诱导心血管交感反射,在α-氯醛糖麻醉猫的 P5-6 穴位进行 EA。单管记录电极插入 NRP 或 rVLM。向 vlPAG 内注射 DL-高半胱氨酸(DLH)可增加 SN 刺激时 NRP 神经元的反应(5±1 到 12±2 个/30 个刺激)。同样,针刺 P5-6 30 分钟可增加 SN 刺激时 NRP 的反应(3±1 到 10±2 个/30 个刺激),该效应可被向 vlPAG 尾侧注射犬尿氨酸(KYN)阻断。此外,向胆囊内给予缓激肽和 SN 刺激 rVLM 心血管节前神经元反应引起的血压反射性升高,被向 vlPAG 内注射 DLH 抑制,该反应可被向 NRP 内注射 KYN 逆转。这些结果表明,EA 激活 vlPAG,vlPAG 兴奋 NRP,进而抑制 rVLM 节前交感神经元和反射性心血管交感兴奋反应。