Huang W, Hoffmann N V, West M J
Department of Medicine, University of Queensland, Prince Charles Hospital, Brisbane.
Aust N Z J Med. 1997 Aug;27(4):479-84. doi: 10.1111/j.1445-5994.1997.tb02222.x.
Intrathecal administration of the specific glutamate subtype receptor agonist NMDA (N-methyl-D-aspartate), or the non-NMDA receptor agonist AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid), at the level of the lower thoracic spinal cord in the conscious rabbit, produces increased levels of plasma norepinephrine and a rise in blood pressure. These responses are specifically inhibited with prior intrathecal administration of the NMDA receptor antagonist AP-5 (2-amino-5-phosphonovaleric acid) or non-NMDA receptor antagonist DNQX (6, 7-dinitroquinoxaline-2, 3-dione), respectively. In contrast, arterial baroreflex activation induced by transient hypotension following intravenous sodium nitroprusside increases levels of plasma norepinephrine which are inhibited with intrathecal AP-5, but not DNQX. The experiments are consistent with glutamate acting as a neurotransmitter in the spinal cord influencing control of sympathetic nerve function via activation of spinal cord NMDA and non-NMDA subtype receptors. The results support previous work suggesting that baroreflex function is predominantly mediated by spinal NMDA receptors and that spinal glutamate receptors are important in baroreflex control of the circulation.
在清醒家兔的下胸段脊髓水平鞘内注射特定的谷氨酸亚型受体激动剂NMDA（N-甲基-D-天冬氨酸）或非NMDA受体激动剂AMPA（α-氨基-3-羟基-5-甲基-4-异恶唑丙酸），会使血浆去甲肾上腺素水平升高以及血压上升。这些反应分别会被事先鞘内注射NMDA受体拮抗剂AP-5（2-氨基-5-磷酸戊酸）或非NMDA受体拮抗剂DNQX（6,7-二硝基喹喔啉-2,3-二酮）特异性抑制。相比之下，静脉注射硝普钠后短暂性低血压诱导的动脉压力反射激活会使血浆去甲肾上腺素水平升高，而这种升高会被鞘内注射AP-5抑制，但不会被DNQX抑制。这些实验表明，谷氨酸作为脊髓中的一种神经递质，通过激活脊髓NMDA和非NMDA亚型受体来影响交感神经功能的控制。这些结果支持了先前的研究工作，表明压力反射功能主要由脊髓NMDA受体介导，并且脊髓谷氨酸受体在压力反射对循环的控制中很重要。
