CAJ | 학술논문

目的：研究尾静脉、蛛网膜下腔注射NK-1受体拮抗剂GR82334对强电流刺激大鼠隐神经（SN）增加扣带回前部（ACG）多巴胺含量的影响。方法将雄性Wistar大鼠42只随机分为空白对照组、假刺激对照组、SN刺激组、GR82334（ith）组、NS（ith）组、GR82334（iv）组及NS（iv）组。将各组大鼠断头后，取出右侧ACG，称质量，加入适量冰冷的0.1 mol/L高氯酸溶液，匀浆，4℃、10000 r/min离心20 min。取上清液20μL，应用高效液相色谱-电化学检测技术检测ACG多巴胺含量。结果强电流刺激SN引起ACG多巴胺含量显著增高；尾静脉或蛛网膜下腔注射GR82334拮抗了强电流刺激SN引起的ACG多巴胺含量的显著增高。蛛网膜下腔注射GR82334未能完全阻断强电流刺激SN引起的ACG多巴胺含量的显著增高。结论外周NK-1受体和中枢NK-1受体参与SN传入信息引起的ACG多巴胺含量显著增高的过程；还存在其它递质和受体参与的中枢通路引起ACG多巴胺含量的显著增高。
목적：연구미정맥、주망막하강주사NK-1수체길항제GR82334대강전류자격대서은신경（SN）증가구대회전부（ACG）다파알함량적영향。방법장웅성Wistar대서42지수궤분위공백대조조、가자격대조조、SN자격조、GR82334（ith）조、NS（ith）조、GR82334（iv）조급NS（iv）조。장각조대서단두후，취출우측ACG，칭질량，가입괄량빙랭적0.1 mol/L고록산용액，균장，4℃、10000 r/min리심20 min。취상청액20μL，응용고효액상색보-전화학검측기술검측ACG다파알함량。결과강전류자격SN인기ACG다파알함량현저증고；미정맥혹주망막하강주사GR82334길항료강전류자격SN인기적ACG다파알함량적현저증고。주망막하강주사GR82334미능완전조단강전류자격SN인기적ACG다파알함량적현저증고。결론외주NK-1수체화중추NK-1수체삼여SN전입신식인기적ACG다파알함량현저증고적과정；환존재기타체질화수체삼여적중추통로인기ACG다파알함량적현저증고。
Objective To investigate the effects of GR82334 caudal veins injection(iv)or intrathecal injection(ith)on the increase of dopamine (DA)content in rats anterior cingulate gyrus(ACG)induced by heavy current stimulation of saphenous nerve(SN). Methods Totally 42 male Wi-star rats were randomly divided into six groups,including control group,sham stimulation group,SN stimulation group,GR82334(ith)group,NS (ith)group,GR82334(iv)group,and NS(iv)group. At the end of the study,rats of different groups were sacrificed,then the right side ACG were collected and weighted. ACG samples were then homogenized with 0.1 mol/L perchloric acid solution. After spinning at 10 000 r/min(4℃)for 20 min,20μL of the supernatant were harvest from each sample. High performance liquid chromatography electrochemical detection was used to mea-sure DA content. Results Heavy current stimulation of SN caused obvious increase of the DA content in ACG. GR82334(iv or ith)antagonized the significant increase of DA content in ACG induced by the stimulating SN. However,GR82334(ith)did not completely antagonized the increase of DA content in ACG induced by electric stimulating SN. Conclusion The results indicated that there is connection between SN and the dopami-nergic nervous system in ACG,and SN afferent nociceptive signals can activate ACG dopaminergic neurons to release DA. Peripheral and central NK-1 receptors are involved in the process of significant increase of DA content in ACG induced by SN afferent signals. However,there are other central paths of SN information input to ACG to induce obvious increases of DA content,in which other neurotransmitters and receptors may be involved.