Roder S, Ciriello J
Department of Physiology Health Science Centre University of Western Ontario, London, Canada.
J Auton Nerv Syst. 1993 Oct;45(1):61-75. doi: 10.1016/0165-1838(93)90362-x.
Anatomical and physiological studies were done in the rat to investigate the possibility that the cardiovascular responses elicited by stimulation of central nucleus of the amygdala (ACe) were mediated via projections to bed nucleus of the stria terminalis (BST). In the first series, to determine the distribution of neurons in ACe that projected to the cardiovascular region of BST, the retrograde tracer Fluorogold (FG) or rhodamine latex micro-beads (Rd) were injected into BST. FG and Rd injections that overlapped the cardiovascular region of BST resulted in retrogradely labelled neurons throughout the amygdala. In ACe, retrogradely labelled neurons were observed primarily in the lateral subdivision of the rostral ACe compared to the caudal ACe. The medial subdivision of ACe was found to have very few retrogradely labelled neurons. In the second series, the effect of either blocking synaptic transmission in BST with CoCl2, chemical lesions of BST with ibotenic acid (IBO), or electrolytic lesions of BST on the depressor response elicited by either electrical or chemical stimulation of ACe was investigated in the chloralose-anesthetized, artificially ventilated and paralysed rat. Microinjections of CoCl2 into BST significantly attenuated the depressor responses to stimulation of the rostral components of the lateral subnucleus of ACe, but not those to stimulation of the caudal and medial components of ACe. Microinjections of IBO into BST or electrolytic lesions of BST resulted in similar effects on the depressor responses to ACe stimulation. Taken together, these data indicate that neurons within the rostral components of the lateral subnucleus of ACe project to the cardiovascular region of BST and mediate in part the depressor responses to stimulation of the rostral ACe. On the other hand, the depressor responses elicited from the caudal ACe are not mediated through BST. These results suggest that at least two independent pathways originate in the ACe that influence the circulation.
在大鼠身上进行了解剖学和生理学研究，以探讨刺激杏仁核中央核（ACe）引发的心血管反应是否通过投射到终纹床核（BST）来介导。在第一组实验中，为了确定ACe中投射到BST心血管区域的神经元分布，将逆行示踪剂荧光金（FG）或罗丹明乳胶微珠（Rd）注射到BST中。与BST心血管区域重叠的FG和Rd注射导致整个杏仁核中出现逆行标记的神经元。在ACe中，与尾侧ACe相比，主要在吻侧ACe的外侧亚区观察到逆行标记的神经元。发现ACe的内侧亚区逆行标记的神经元很少。在第二组实验中，在氯醛糖麻醉、人工通气和麻痹的大鼠中，研究了用CoCl2阻断BST中的突触传递、用鹅膏蕈氨酸（IBO）进行BST的化学损伤或BST的电解损伤对电刺激或化学刺激ACe引起的降压反应的影响。向BST中微量注射CoCl2显著减弱了对刺激ACe外侧亚核吻侧部分的降压反应，但对刺激ACe尾侧和内侧部分的降压反应没有影响。向BST中微量注射IBO或BST的电解损伤对ACe刺激的降压反应产生了类似的影响。综上所述，这些数据表明，ACe外侧亚核吻侧部分的神经元投射到BST的心血管区域，并部分介导对刺激吻侧ACe的降压反应。另一方面，尾侧ACe引起的降压反应不是通过BST介导的。这些结果表明，至少有两条独立的通路起源于ACe，影响循环系统。
