Prolonged stimulation of respiration by brain stem metabotropic glutamate receptors.
Prolonged stimulation of respiration by brain stem metabotropic glutamate receptors.
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脑干代谢型谷氨酸受体长时间刺激呼吸。
DOI：
10.1152/jappl.1995.79.5.1650
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Nattie,EE
中科院分区：
文献类型：
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作者：
Li,A;Nattie,EE
氨环戊二甲酸[(1S,3R)-ACPD]对氯氯脲麻醉大鼠后锥体核（RTN）代谢性谷氨酸受体（mGluRs）的刺激作用10 nl， 1 mM]增加综合膈神经振幅（PNA），持续bbbb60 min。在这里，我们想知道mGluR拮抗剂(+-)- α -甲基-4-羧基苯基甘氨酸[(+-)- mcpg]是否可以阻断这种作用。使用多管微移液器，我们首先通过观察短时间注射谷氨酸（10 nl, 100 mM）（一种假定的嗜离子受体反应）对PNA产生的短暂刺激，确定了影响呼吸的RTN位点。然后在同一部位注射(+-)- mcpg的活性或非活性异构体（10 nl, 10 mM），然后注射(1S,3R)- acpd或长时间（60 s）注射谷氨酸（10 nl, 100 mM）。对每个注射部位进行解剖验证。活性拮抗剂(+-)- mcpg本身对PNA无显著影响，但可阻断1)随后（1S,3R)- acpd诱导的PNA刺激99 +/- 11 (SE) min, 2） 60 s谷氨酸注射后PNA反应66 +/- 6 min。失活形式(-)- mcpg对(1S,3R)- acpd诱导的PNA刺激无影响。我们得出结论：1)RTN mGluRs可能参与呼吸控制，2)RTN mGluRs在呼吸暂停时不活跃，3)刺激RTN mGluRs可能需要延长谷氨酸释放时间。
Stimulation of metabotropic glutamate receptors (mGluRs) in the retrotrapezoid nucleus (RTN) of chloralose-urethan-anesthetized rats by the mGluR agonist (1S,3R)-aminocyclopentanedicarboxylic acid [(1S,3R)-ACPD; 10 nl, 1 mM] increases integrated phrenic nerve amplitude (PNA) for > 60 min. Here we ask if the mGluR antagonist (+-)-alpha-methyl-4-carboxyphenylglycine [(+-)-MCPG] can block this effect. Using multibarreled micropipettes, we first identified RTN sites that affect respiration by noting short-lived stimulation of PNA produced by brief-duration injection of glutamate (10 nl, 100 mM), a presumed ionotropic receptor response. We then injected the active or inactive isomer of (+-)-MCPG (10 nl, 10 mM) followed by (1S,3R)-ACPD or by a long-duration (60-s) injection of glutamate (10 nl, 100 mM) at the same site. Each injection location was verified anatomically. The active antagonist (+-)-MCPG itself had no significant effect on PNA, but it blocked 1) subsequent (1S,3R)-ACPD-induced PNA stimulation for 99 +/- 11 (SE) min and 2) the PNA response to 60-s glutamate injection for 66 +/- 6 min. The inactive form (-)-MCPG had no effect on (1S,3R)-ACPD-induced PNA stimulation. We conclude that 1) RTN mGluRs may be involved in respiratory control, 2) RTN mGluRs are not active in eupnea, and 3) stimulation of RTN mGluRs may require prolonged glutamate release.