Lewis S J, Verberne A J, Robinson T G, Jarrott B, Louis W J, Beart P M
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Vic. Australia.
Brain Res. 1989 Aug 14;494(2):232-40. doi: 10.1016/0006-8993(89)90591-x.
The present study has examined the influence of the central nucleus of the amygdala (Ce) and the basolateral nucleus of the amygdala (BL) on the baroreceptor heart rate (HR) reflex in conscious, unrestrained rats. Baroreceptor HR reflex activity was examined in rats with bilateral excitotoxin (N-methyl-D-aspartate; 40 nmol/side)-induced lesions of the Ce or the BL and in control rats (artificial cerebrospinal fluid). After lesioning, the reflex HR responses were recorded following intravenous bolus doses of the pressor agent phenylephrine and the depressor agent sodium nitroprusside. Baroreceptor reflex parameters were determined by sigmoidal computerized curve-fitting. Lesions of either the Ce or the BL failed to affect resting mean arterial pressure (MAP) or HR. However, the Ce lesion reduced the maximum and average gain (sensitivity) of the baroreceptor reflex, and diminished the range of the reflex by altering the minimum, but not the maximum HR plateau. The upper and lower reflex thresholds and the MAP value corresponding to the midpoint of the HR range were not affected. Bilateral lesions of the BL failed to modify any baroreceptor reflex parameters. These results suggest that despite previous evidence for the involvement of the BL in cardiovascular regulation this nucleus does not exert a tonic influence on vasomotor neurons nor does it influence the baroreceptor HR reflex. In contrast, neurons projecting from the Ce appear to provide excitatory input to medullary neurons involved in baroreceptor reflex are regulation.
本研究检测了杏仁核中央核(Ce)和杏仁核基底外侧核(BL)对清醒、自由活动大鼠压力感受器心率(HR)反射的影响。在双侧经兴奋性毒素(N-甲基-D-天冬氨酸;40 nmol/侧)诱导Ce或BL损伤的大鼠以及对照大鼠(人工脑脊液)中检测压力感受器HR反射活动。损伤后,在静脉注射升压药去氧肾上腺素和降压药硝普钠后记录反射性HR反应。通过S形计算机曲线拟合确定压力感受器反射参数。Ce或BL损伤均未影响静息平均动脉压(MAP)或HR。然而,Ce损伤降低了压力感受器反射的最大和平均增益(敏感性),并通过改变最小而非最大HR平台期减小了反射范围。上下反射阈值以及与HR范围中点对应的MAP值未受影响。BL双侧损伤未改变任何压力感受器反射参数。这些结果表明,尽管先前有证据表明BL参与心血管调节,但该核团对血管运动神经元没有紧张性影响,也不影响压力感受器HR反射。相反,从Ce投射的神经元似乎为参与压力感受器反射调节的延髓神经元提供兴奋性输入。