NMDA and GABAA receptors in the rat Kolliker-Fuse area control cardiorespiratory responses evoked by trigeminal ethmoidal nerve stimulation
NMDA and GABAA receptors in the rat Kolliker-Fuse area control cardiorespiratory responses evoked by trigeminal ethmoidal nerve stimulation
复制标题
DOI：
10.1111/j.1469-7793.1998.793bj.x
复制
发表时间：
1998-08-01
影响因子：
5.5
通讯作者：
Herbert, H
中科院分区：
文献类型：
--
作者：
Dutschmann, M;Herbert, H
1. 筛神经（EN5）的电刺激（10秒）引起鼻三叉神经反射反应，包括呼吸暂停、心动过缓和动脉血压升高。在本研究中，我们检查了 Kolliker-Fuse (KP) 核中 N-甲基-D-天冬氨酸 (NMDA)、AMPA/红藻氨酸、(γ-氨基丁酸 (A) (GBBA(A)) 和甘氨酸受体在鼻三叉神经反射反应介导中的参与情况。2. 单侧注射 (n = 6) 50-100 nl NMDA 受体拮抗剂 AP5 KF 区域导致 EN5 诱发的呼吸抑制和心动过缓的显着阻断最有效（阻断 80-90%），动脉血压的升高不受影响。3. 单侧注射 AMPA/红藻氨酸受体拮抗剂 CNQX 未能显着阻断 EN5 诱发的自主反应。 = 5) 的 GABA(A) 受体拮抗剂荷包牡丹碱可增强 EN5 引起的呼吸抑制和心动过缓，在刺激 KF 区域的中层后，效果持续长达 30 秒，动脉血压的升高仍然不受影响。 5. 单侧注射甘氨酸受体拮抗剂士的宁对 KF 区域没有产生任何显着影响。 EN5 诱发的自主反应。6. 我们的结果表明，KF 区域代表了鼻三叉神经引起的呼吸暂停和心动过缓的强制中继，这些呼吸暂停和心动过缓主要由 KF 中的 NMDA 受体介导。此外，EN5 诱发的动脉血压升高似乎不受任何药物的影响，因此似乎不是通过 KF 介导的。
1. Electrical stimulation (10 s) of the ethmoidal nerve (EN5) evokes the nasotrigeminal reflex responses, including apnoea, bradycardia and rise in arterial blood pressure. In the present study, we examined the involvement of N-methyl-D-aspartate (NMDA), AMPA/kainate, (gamma-aminobutyric acid(A) (GBBA(A)) and glycine receptors in the Kolliker-Fuse (KP) nucleus in the mediation of the nasotrigeminal reflex responses.2. Unilateral injections (n = 6) of 50-100 nl of the NMDA receptor antagonist AP5 into the KF area led to a significant blockade of the EN5-evoked respiratory depression and bradycardia. Injections placed into the midlevel of the KP area were most effective (80-90% blockade). The rise in arterial blood pressure remained unaffected.3. Unilateral injections (n = 6) of the AMPA/kainate receptor antagonist CNQX into the KP area failed to block EN5-evoked autonomic responses significantly.4. Unilateral injections (n = 5) of the GABA(A) receptor antagonist bicuculline enhanced the EN5-evoked respiratory depression and bradycardia. The effect persisted for up to 30 s after stimulation. Bicuculline injections into the midlevel of the KF area were most effective. The increase in arterial blood pressure remained unaffected.5. Unilateral injections (n = 5) of the glycine receptor antagonist strychnine into the KF area did not produce any significant effects on EN5-evoked autonomic responses.6. Our results suggest that the KF area represents a mandatory relay for the nasotrigeminally induced apnoea and bradycardia which are predominantly mediated by NMDA receptors in the KF. Furthermore, it appears that IIB neurons are under a potent GABAergic inhibitory control. The EN5-evoked rise in arterial blood pressure was not altered by any of the drugs and, therefore, appears not to be mediated via the KF.