Miyawaki T, Suzuki S, Minson J, Arnolda L, Chalmers J, Llewellyn-Smith I, Pilowsky P
Department of Medicine, Flinders Medical Centre, Bedford Park, South Australia.
Am J Physiol. 1997 Mar;272(3 Pt 2):R800-12. doi: 10.1152/ajpregu.1997.272.3.R800.
We examined the role of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors within the caudal ventrolateral medulla (CVLM) in mediating the sympathetic baroreceptor reflex in anesthetized and paralyzed rats. Bilateral microinjection into CVLM of either DL-2-amino-5-phosphonovaleric acid [APV; a selective N-methyl-D-aspartic acid (NMDA) receptor antagonist, 20 mM, 100 nl] or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; a selective AMPA/kainate receptor antagonist, 2 mM, 100 nl) alone failed to eliminate the aortic nerve stimulation-evoked hypotension and inhibition of splanchnic sympathetic nerve activity (SNA) or the cardiac-related rhythmicity of SNA. All components of the sympathetic-baroreceptor reflex were abolished when kynurenate (100 mM, 30 nl) or mixtures of APV and CNQX (10 and 1 mM, respectively, 100 or 30 nl) were injected into CVLM. Injection of APV or CNQX into CVLM reduced aortic nerve-evoked inhibitory responses of bulbospinal sympathoexcitatory neurons in rostral ventrolateral medulla (RVLM). The extent of this reduction was variable. Usually, significant inhibition was preserved. In seven RVLM neurons, intravenous injection of MK-801 (NMDA receptor antagonist, 2 mg/kg) failed to eliminate aortic nerve-evoked inhibitory responses. However, inhibitory responses were abolished when CNQX was injected into CVLM after intravenous MK-801. We conclude that both NMDA and AMPA/kainate receptors in CVLM transmit baroreceptor information.
我们研究了尾侧腹外侧延髓（CVLM）内的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）/海人藻酸受体在介导麻醉和麻痹大鼠的交感压力感受器反射中的作用。单独向CVLM双侧微量注射DL-2-氨基-5-磷酸戊酸[APV；一种选择性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂，20 mM，100 nl]或6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX；一种选择性AMPA/海人藻酸受体拮抗剂，2 mM，100 nl）未能消除主动脉神经刺激诱发的低血压和内脏交感神经活动（SNA）抑制或SNA的心脏相关节律性。当向CVLM注射犬尿氨酸（100 mM，30 nl）或APV和CNQX的混合物（分别为10和1 mM，100或30 nl）时，交感压力感受器反射的所有成分均被消除。向CVLM注射APV或CNQX可降低延髓头端腹外侧（RVLM）中延髓脊髓交感兴奋神经元的主动脉神经诱发的抑制反应。这种降低的程度是可变的。通常，仍保留显著抑制作用。在7个RVLM神经元中，静脉注射MK-801（NMDA受体拮抗剂，2 mg/kg）未能消除主动脉神经诱发的抑制反应。然而，在静脉注射MK-801后向CVLM注射CNQX时，抑制反应被消除。我们得出结论，CVLM中的NMDA和AMPA/海人藻酸受体均传递压力感受器信息。
