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代谢型谷氨酸受体抑制孤束核中迷走神经和主动脉压力感受器的信号传递。

Metabotropic glutamate receptors depress vagal and aortic baroreceptor signal transmission in the NTS.

作者信息

Liu Z, Chen C Y, Bonham A C

机构信息

Division of Cardiovascular Medicine and Department of Pharmacology, University of California, Davis, California 95616, USA.

出版信息

Am J Physiol. 1998 Nov;275(5):H1682-94. doi: 10.1152/ajpheart.1998.275.5.H1682.

DOI:10.1152/ajpheart.1998.275.5.H1682
PMID:9815076
Abstract

We sought to determine whether metabotropic glutamate receptors contribute to frequency-dependent depression of vagal and aortic baroreceptor signal transmission in the nucleus of the solitary tract (NTS) in vivo. In alpha-chloralose-anesthetized rabbits, we determined the number of extracellular action potentials synaptically evoked by low (1 Hz)- or high-frequency vagal (3-20 Hz) or aortic depressor nerve (ADN) (6-80 Hz) stimulation and postsynaptically evoked by the ionotropic glutamate receptor agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). The metabotropic glutamate receptor agonist (2S,1'S, 2'S)-2-(carboxycyclopropyl)glycine (L-CCG-I) attenuated NTS responses monosynaptically evoked by 1-Hz vagus stimulation by 34% (n = 25; P = 0.011), while augmenting AMPA-evoked responses by 64% (n = 17; P = 0.026). The metabotropic glutamate receptor antagonist alpha-methyl-4-phosphonophenylglycine (MPPG) did not affect NTS responses to low-frequency vagal stimulation (n = 11) or AMPA (n = 10) but augmented responses to high-frequency stimulation by 50% (n = 25; P = 0.0001). MPPG also augmented NTS responses to high-frequency ADN stimulation by 35% (n = 9; P = 0.048) but did not affect responses to low-frequency stimulation (n = 9) or AMPA (n = 7). The results suggest that metabotropic glutamate receptors, presumably at presynaptic sites, contribute to frequency-dependent depression of vagal and aortic baroreceptor signal transmission in NTS.

摘要

我们试图确定代谢型谷氨酸受体是否在体内孤束核(NTS)中对迷走神经和主动脉压力感受器信号传递的频率依赖性抑制起作用。在α-氯醛糖麻醉的兔子中,我们确定了由低频(1Hz)或高频迷走神经(3 - 20Hz)或主动脉减压神经(ADN)(6 - 80Hz)刺激突触诱发的细胞外动作电位数量,以及由离子型谷氨酸受体激动剂α-氨基-3-羟基-5-甲基异恶唑-4-丙酸(AMPA)突触后诱发的动作电位数量。代谢型谷氨酸受体激动剂(2S,1'S,2'S)-2-(羧基环丙基)甘氨酸(L-CCG-I)使1Hz迷走神经刺激单突触诱发的NTS反应减弱34%(n = 25;P = 0.011),同时使AMPA诱发的反应增强64%(n = 17;P = 0.026)。代谢型谷氨酸受体拮抗剂α-甲基-4-膦酰苯甘氨酸(MPPG)不影响NTS对低频迷走神经刺激(n = 11)或AMPA(n = 10)的反应,但使对高频刺激的反应增强50%(n = 25;P = 0.0001)。MPPG还使NTS对高频ADN刺激的反应增强35%(n = 9;P = 0.048),但不影响对低频刺激(n = 9)或AMPA(n = 7)的反应。结果表明,代谢型谷氨酸受体可能在突触前位点,对NTS中迷走神经和主动脉压力感受器信号传递的频率依赖性抑制起作用。

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