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在下唇,孤啡肽信号转导在副交感反射性血管舒张中的作用。

Role of medullary GABA signal transduction on parasympathetic reflex vasodilatation in the lower lip.

机构信息

Division of Dento-oral Anesthesiology, Department of Tohoku University Graduate School of Dentistry, 4-1 Seiryo-machi, Aoba, Sendai 980-8575, Japan.

出版信息

Brain Res. 2012 Feb 9;1437:26-37. doi: 10.1016/j.brainres.2011.12.023. Epub 2011 Dec 20.

DOI:10.1016/j.brainres.2011.12.023
PMID:22226507
Abstract

In the orofacial area, noxious stimulation of the orofacial structure in the trigeminal region evokes parasympathetic reflex vasodilatation, which occurs via the trigeminal spinal nucleus (Vsp) and the inferior/superior salivatory nucleus (ISN/SSN). However, the neurotransmitter involved in the inhibitory synaptic inputs within these nuclei has never been described. This parasympathetic reflex vasodilatation is suppressed by GABAergic action of volatile anesthetics, such as isoflurane, sevoflurane, and halothane, suggesting that medullary GABAergic mechanism exerts its inhibitory effect on the parasympathetic reflex via an activation of GABA receptors. The aim of the present study was to determine the role of GABA(A) and GABA(B) receptors in the Vsp and the ISN in regulating the lingual nerve (LN)-evoked parasympathetic reflex vasodilatation in the lower lip. Under urethane anesthesia (1g/kg), change in lower lip blood flow elicited by electrical stimulation of the LN was recorded in cervically vago-sympathectomized rats. Microinjection of GABA (10 μM; 0.3 μl/site) into the Vsp or the ISN significantly and reversibly attenuated the LN-evoked parasympathetic reflex vasodilatation. Microinjection of the GABA(A) receptor-selective agonist muscimol (100 μM; 0.3 μl/site) or the GABA(B) receptor-selective agonist baclofen (100 μM; 0.3 μl/site) into the Vsp or the ISN significantly and irreversibly reduced this reflex vasodilatation, and these effects were attenuated by pretreatment with microinjection of each receptor-selective antagonists [GABA(A) receptor selective antagonist bicuculline methiodide (1mM; 0.3 μl/site) or GABA(B) receptor selective antagonist CGP-35348 (1mM; 0.3 μl/site)] into the Vsp or the ISN. Microinjection of these antagonists alone into the Vsp or the ISN had no significant effect on this reflex vasodilatation. In addition, microinjection (0.3 μl/site) of the mixture of muscimol (100 μM) and baclofen (100 μM) into the Vsp or the ISN also significantly reduced this reflex vasodilatation. These results suggest that medullary GABA signal transduction inhibits the parasympathetic reflex vasodilatation in the rat lower lip via GABA(A) and GABA(B) receptors in the Vsp and the ISN.

摘要

在头面部区域,三叉神经区域的口腔结构的有害刺激会引起副交感反射性血管扩张,这是通过三叉神经脊髓核(Vsp)和下/上涎核(ISN/SSN)发生的。然而,这些核内抑制性突触输入所涉及的神经递质从未被描述过。这种副交感反射性血管扩张被挥发性麻醉剂(如异氟烷、七氟烷和氟烷)的 GABA 能作用所抑制,这表明髓质 GABA 能机制通过激活 GABA 受体对副交感反射施加抑制作用。本研究的目的是确定 GABA(A)和 GABA(B)受体在 Vsp 和 ISN 中在调节舌神经(LN)诱发的下唇副交感反射性血管扩张中的作用。在氨基甲酸乙酯麻醉(1g/kg)下,记录颈部迷走神经-交感神经切断大鼠 LN 电刺激引起的下唇血流变化。将 GABA(10 μM;0.3 μl/部位)微注射到 Vsp 或 ISN 中可显著和可逆地减弱 LN 诱发的副交感反射性血管扩张。将 GABA(A)受体选择性激动剂 muscimol(100 μM;0.3 μl/部位)或 GABA(B)受体选择性激动剂 baclofen(100 μM;0.3 μl/部位)微注射到 Vsp 或 ISN 中可显著和不可逆地降低这种反射性血管扩张,并且这些作用可通过预先微注射各受体选择性拮抗剂 [GABA(A)受体选择性拮抗剂bicuculline methiodide(1mM;0.3 μl/部位)或 GABA(B)受体选择性拮抗剂 CGP-35348(1mM;0.3 μl/部位)]来减弱。将这些拮抗剂单独微注射到 Vsp 或 ISN 中对这种反射性血管扩张没有显著影响。此外,将 muscimol(100 μM)和 baclofen(100 μM)混合物(0.3 μl/部位)微注射到 Vsp 或 ISN 中也显著降低了这种反射性血管扩张。这些结果表明,通过 Vsp 和 ISN 中的 GABA(A)和 GABA(B)受体,髓质 GABA 信号转导抑制大鼠下唇的副交感反射性血管扩张。

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