- 期刊
Neurons in the Medullary Gigantocellular Reticular Nucleus Mediate Cardioinhibition in Cats
延腦巨大細胞網狀核引發心跳變慢作用的神經細胞機構
摘要
在氯醛醣及氨甲酸乙酯麻醉的貓，在其延腦的巨大細胞網狀核用0.5M胅氨酸鈉作微量(100nl)注射，觀察其心跳變慢情形，並在該地區行神經細胞外電位活動記錄，以進一步探討巨大細胞網狀核細胞的神經性心跳變慢機構。 結果發現，在巨大細胞網狀核分佈注射胅氨酸鈉能引發心跳變慢反應，其引發心跳變慢的效果，以在該核的頭端（在上橄欖核之頭端）較尾端為佳，暗示該神經核具有能引發心跳變慢的細胞，而這些細胞又以存在於頭端較多。 在巨大網狀核行細胞外電記錄，一共觀察到78個細胞。在60個巨大網狀核的神經細胞中、曾對其電活動情形與心律，及由靜脈注射正腎上腺素、或三硝酸甘油酯所引起的血壓上升或下降之間的關係加以探討，發現其中45%(27/60)細胞，其電活動情形與血壓之升降相關，而2.5%(15/60)細胞則與心律相關。61個巨大網狀細胞中，曾用逆向激發方法探測其是否有向迷走神經背核及獨孤核作軸突投射，結果發現18%(11/60)之細胞、其細胞電活動能因迷走神經背核及獨孤二核被刺激所激發，亦即巨大網狀細胞之軸突有向迷走神經背核及獨孤核投射情形。 由上所得到的結果，推論：1.在巨大細胞網狀核中具有抑心作用的細胞存在。2.這些神經細胞可能是經由迷走神經背核及獨孤核之感壓反射機構，產生心跳變慢反應。
關鍵字
無資料並列摘要
Su, C.K., C.T. Yen, C.Y. Chai, and J.S.Kuo, Neurons in the medullary gigantocellular reticular nucleus mediate cardioinhibition in cats. Chinese J. Physiol. 3 4(4): 399-4 12, 1991. The cardioinhibitory mechanisms (bradycardia) of the gigantocellular reticular nucleus (GRN) of medulla was studied in chloralose-urethane anesthetized cats by means of micro- injection of sodium glutamate (0.5M, 100nl) and single neuron recording. Microinjection of glutamate excited the GRN neurons and produced the bradycardiac responses. The rostral GRN (rostral to the caudal superior olivary nucleus) had higher proportion of bradycardiac loci than the caudal GRN. This suggests that the density of cardioinhibitory neurons in GRN is higher in the rostral than the caudal level. Seventy-eight GRN neurons were recorded extracellularly. Activities of 60 neurons were tested if they were correlated with cardiac rhythm or systemic arterial blood pressure (SAP) changes following intravenous norepinephrine or nitroglycerin. Among these neurons 45% (27/60) exhibited changes related to SAP and 25% (15/60) related to cardiac rhythm. Sixty-one GRN neurons were tested by antidromic activation to determine whether they have axonal projection to the dorsal motor nucleus of vagus and nucleus tractus solitarius (DMN/NTS). Eighteen percent (11/61) of them had axonal projections to the DMN/NTS. These findings suggest that: (i) In GRN there are neurons which mediate cardioinhibition. (ii) These neurons may receive baroreceptor inputs. (iii) They may decrease heart rate through the DMN/NTX.