BACKGROUND： A large number of investigations have shown that acetylcholine （ACh） and the nucleus locus coeruleus （LC） play an important role in the modulation of pain in rats; however, there is no concrete eviden...BACKGROUND： A large number of investigations have shown that acetylcholine （ACh） and the nucleus locus coeruleus （LC） play an important role in the modulation of pain in rats; however, there is no concrete evidence addressing the relationship between ACh injection into the LC and the electrical activities of pain-related neurons in the LC of healthy rats. OBJECTIVE： To study changes in the discharge of pain-related neurons in the LC following injection of ACh, or its M receptor antagonist, atropine, and to investigate the role of ACh and the LC in the pain signaling pathway. DESIGN, TIME AND SETTING： A randomized, controlled, neuroelectrophysiological animal experiment was performed from November 2007 to December 2008, in the Physiological Laboratory of Harbin Medical University, China. MATERIALS： Acetylcholine chloride was obtained from Shanghai San＇aisi Reagent Co., Ltd., China atropine was purchased from Tianjin Jinyao Amino Acid Co., Ltd., China. METHODS： This study was divided into two sections as follows： （1） 46 adult Wistar rats were randomly assigned into an ACh group and a control group, with 23 rats in each. （2） 34 adult Wistar rats were randomly assigned to an atropine group and a control group, with 17 rats in each. The sciatic nerve was stimulated by a series of electrical impulses, serving as peripheral noxious stimuli. Electrical changes in pain-related neurons in the LC were measured by glass microelectrodes. The LC of rats in the ACh and atropine groups were injected with 2 μg/μL ACh or 0.5 μg/μL atropine, respectively, in 1 μL volume. Rats in the control groups received injection of 1 pL physiological saline within 4 minutes. MAIN OUTCOME MEASURES： To measure the net increase in the discharge value, latency and complete inhibitory duration of pain-related neurons before and after administration of ACh or atropine. RESULTS： The injection of ACh into the LC increased the pain-evoked discharge frequency and shortened the latency of the pain-excitation neurons. It decreased the pain-evoked discharged frequency and prolonged the inhibitory duration of pain-inhibition neurons. Injection of atropine into LC blocked the effects of ACh. CONCLUSION： ACh strengthened the response of pain-related neurons in LC of rats to noxious stimulation, exhibiting the effects of facilitated pain. This indicates that ACh and LC play an important role in the modulation of algesia.展开更多
基金the National Natural Science Foundation of China,No.30240058
文摘BACKGROUND： A large number of investigations have shown that acetylcholine （ACh） and the nucleus locus coeruleus （LC） play an important role in the modulation of pain in rats; however, there is no concrete evidence addressing the relationship between ACh injection into the LC and the electrical activities of pain-related neurons in the LC of healthy rats. OBJECTIVE： To study changes in the discharge of pain-related neurons in the LC following injection of ACh, or its M receptor antagonist, atropine, and to investigate the role of ACh and the LC in the pain signaling pathway. DESIGN, TIME AND SETTING： A randomized, controlled, neuroelectrophysiological animal experiment was performed from November 2007 to December 2008, in the Physiological Laboratory of Harbin Medical University, China. MATERIALS： Acetylcholine chloride was obtained from Shanghai San＇aisi Reagent Co., Ltd., China atropine was purchased from Tianjin Jinyao Amino Acid Co., Ltd., China. METHODS： This study was divided into two sections as follows： （1） 46 adult Wistar rats were randomly assigned into an ACh group and a control group, with 23 rats in each. （2） 34 adult Wistar rats were randomly assigned to an atropine group and a control group, with 17 rats in each. The sciatic nerve was stimulated by a series of electrical impulses, serving as peripheral noxious stimuli. Electrical changes in pain-related neurons in the LC were measured by glass microelectrodes. The LC of rats in the ACh and atropine groups were injected with 2 μg/μL ACh or 0.5 μg/μL atropine, respectively, in 1 μL volume. Rats in the control groups received injection of 1 pL physiological saline within 4 minutes. MAIN OUTCOME MEASURES： To measure the net increase in the discharge value, latency and complete inhibitory duration of pain-related neurons before and after administration of ACh or atropine. RESULTS： The injection of ACh into the LC increased the pain-evoked discharge frequency and shortened the latency of the pain-excitation neurons. It decreased the pain-evoked discharged frequency and prolonged the inhibitory duration of pain-inhibition neurons. Injection of atropine into LC blocked the effects of ACh. CONCLUSION： ACh strengthened the response of pain-related neurons in LC of rats to noxious stimulation, exhibiting the effects of facilitated pain. This indicates that ACh and LC play an important role in the modulation of algesia.
