Nosjean A, Franc B, Laguzzi R
INSERM U288, Neurobiologie Cellulaire et Fonctionnelle, Faculté de Médecine Pitié-Salpêtrière, Paris, France.
Neurosci Lett. 1995 Feb 15;186(1):41-4. doi: 10.1016/0304-3940(95)11277-4.
Previous studies have shown that serotonin3 receptor activation in the nucleus tractus solitarius (NTS) increased mean arterial pressure (MAP) and inhibited the cardiac component of the baroreceptor reflex [9]. We have examined the effects of such stimulation upon spontaneous and evoked sympathetic nerve activity. Microinjection of serotonin (10 nmol) into the NTS of halothane-anaesthetized, paralyzed and artificially ventilated rats produced an increase in MAP and lumbar sympathetic nerve discharge which could be completely prevented by prior local microinjection of zacopride, a potent serotonin3 antagonist (200 pmol). In addition, 1-(m-chlorophenyl)-biguanide, a selective serotonin3 receptor agonist, mimicked the sympathoexcitatory effect of serotonin. Since the gain of the sympathetic component of the baroreflex was unaltered after intra-NTS microinjection of serotonin, it could be concluded that serotonin3 receptors activation in the NTS induces a sympathetic activation which is not mediated through an inhibition of the sympathetic baroreceptor reflex arc.
先前的研究表明，孤束核（NTS）中的5-羟色胺3受体激活会增加平均动脉压（MAP），并抑制压力感受器反射的心脏成分[9]。我们已经研究了这种刺激对自发和诱发的交感神经活动的影响。在氟烷麻醉、麻痹并人工通气的大鼠的NTS中微量注射5-羟色胺（10 nmol）会使MAP和腰交感神经放电增加，而预先在局部微量注射强效5-羟色胺3拮抗剂扎考必利（200 pmol）可完全防止这种情况。此外，选择性5-羟色胺3受体激动剂1-（间氯苯基）-双胍模拟了5-羟色胺的交感兴奋作用。由于在NTS内微量注射5-羟色胺后压力反射的交感成分增益未改变，因此可以得出结论，NTS中的5-羟色胺3受体激活会诱导交感激活，而这种激活不是通过抑制交感压力感受器反射弧介导的。
