Bauer R M, Vela M B, Simon T, Waldrop T G
Department of Physiology and Biophysics, College of Medicine, University of Illinois, Urbana 61801.
Brain Res Bull. 1988 May;20(5):633-41. doi: 10.1016/0361-9230(88)90224-9.
Several laboratories have shown that electrical stimulation in the posterior hypothalamus inhibits the baroreceptor reflex. However, the results of these studies are difficult to interpret since it is not known if the attenuation of the baroreflex results from activation of axons of passage or from stimulation of hypothalamic cell bodies. The purpose of this study was to determine the effects of chemical stimulation of posterior hypothalamic neurons upon the baroreflex. Arterial baroreceptors were activated by increasing the pressure in an isolated carotid sinus in anesthetized cats and by an increased arterial pressure following intravenous injection of phenylephrine in both anesthetized cats and rats. The baroreceptor reflex was evaluated before and after a GABA antagonist (picrotoxin) was microinjected into the posterior hypothalamus. The bradycardia, but not the depressor response, elicited by increasing carotid sinus pressure was attenuated after unilateral microinjections of picrotoxin into the posterior hypothalamus. In addition, the heart rate response to a phenylephrine-evoked rise in arterial pressure was reduced after picrotoxin was microinjected in both the cats and the rats. Microinjection of a GABA agonist (muscimol) into the same hypothalamic site returned resting heart rate and arterial pressure to levels seen prior to picrotoxin. These results show that the depression of the bradycardia produced by hypothalamic stimulation results from activation of cell bodies in the posterior hypothalamus. This hypothalamic effect upon the baroreflex bradycardia may involve a GABAergic mechanism.
多个实验室已表明，下丘脑后部的电刺激会抑制压力感受器反射。然而，这些研究结果难以解释，因为尚不清楚压力反射的减弱是由于过路轴突的激活还是下丘脑细胞体的刺激所致。本研究的目的是确定化学刺激下丘脑后部神经元对压力反射的影响。在麻醉猫中，通过增加离体颈动脉窦内的压力，以及在麻醉猫和大鼠中静脉注射去氧肾上腺素后使动脉压升高来激活动脉压力感受器。在将γ-氨基丁酸（GABA）拮抗剂（苦味毒）微量注射到下丘脑后部之前和之后评估压力感受器反射。在下丘脑后部单侧微量注射苦味毒后，由颈动脉窦压力升高引起的心动过缓（而非降压反应）减弱。此外，在猫和大鼠中微量注射苦味毒后，对去氧肾上腺素引起的动脉压升高的心率反应降低。将GABA激动剂（蝇蕈醇）微量注射到相同的下丘脑部位可使静息心率和动脉压恢复到苦味毒注射前的水平。这些结果表明，下丘脑刺激产生的心动过缓抑制是由于下丘脑后部细胞体的激活所致。下丘脑对压力反射性心动过缓的这种作用可能涉及一种GABA能机制。
