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脑桥N-甲基-D-天冬氨酸受体在大鼠吸气终止中的作用

Involvement of pontile NMDA receptors in inspiratory termination in rat.

作者信息

Fung M L, Wang W, St John W M

机构信息

Department of Physiology, Dartmouth Medical School, Lebanon, NH 03756-0001.

出版信息

Respir Physiol. 1994 May;96(2-3):177-88. doi: 10.1016/0034-5687(94)90125-2.

Abstract

We evaluated the hypothesis that N-methyl-D-aspartate (NMDA) receptors in the rostral pons mediate the off-switch of inspiration in the adult rat. Experiments were performed on decerebrate, vagotomized, paralyzed and ventilated animals. Activity of phrenic nerve was recorded. Small volumes (10 nl) of NMDA antagonists, MK-801 and AP-5, or non-NMDA antagonists, CNQX and DNQX, were injected into the rostral pons. We found that injections of MK-801 reversibly increased the duration of neural inspiration (TI), and the increase was dose-dependent. Injections of AP-5 also increased TI. Injections of the DNQX and CNQX in these same loci resulted in no significant changes in the duration of neural inspiration, expiration or peak phrenic activity (PNA). However, injections of kainic acid (KA, 4.7 mM) in the loci increased TI and decreased PNA. We conclude that neurons regulating the off-switch mechanism are located in the rostral pons. Further, the binding of NMDA receptors in the rostral pons is involved in this off-switch mechanism.

摘要

我们评估了如下假说

成年大鼠延髓嘴侧的N-甲基-D-天冬氨酸(NMDA)受体介导吸气的关闭。实验在去大脑、切断迷走神经、麻痹并通气的动物身上进行。记录膈神经的活动。将小剂量(10 nl)的NMDA拮抗剂MK-801和AP-5或非NMDA拮抗剂CNQX和DNQX注入延髓嘴侧。我们发现,注射MK-801可使神经吸气时长(TI)可逆性增加,且这种增加呈剂量依赖性。注射AP-5也可增加TI。在相同位点注射DNQX和CNQX,神经吸气时长、呼气时长或膈神经活动峰值(PNA)均无显著变化。然而,在位点注射 kainic acid(KA,4.7 mM)可增加TI并降低PNA。我们得出结论,调节关闭机制的神经元位于延髓嘴侧。此外,延髓嘴侧NMDA受体的结合参与了这种关闭机制。

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