Group I metabotropic glutamate receptors on second-order baroreceptor neurons are tonically activated and induce a Na+-Ca2+ exchange current.
Group I metabotropic glutamate receptors on second-order baroreceptor neurons are tonically activated and induce a Na+-Ca2+ exchange current.
复制标题
二阶压力感受器神经元上的 I 类代谢型谷氨酸受体被强直激活并诱导 Na -Ca2 交换电流。
DOI：
10.1152/jn.00772.2005
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发表时间：
2006
影响因子：
2.5
通讯作者：
Bonham,AnnC
中科院分区：
文献类型：
--
作者：
Sekizawa,Shin-ichi;Bonham,AnnC
孤束核（NTS）是协调压力反射控制血压的关键。压力感受器感觉纤维在二级NTS神经元上形成突触。谷氨酸溢出激活压力感受器中央末梢上的组II和III突触前代谢型谷氨酸受体（mGluRs）以抑制突触传递，但突触后mGluRs的作用尚不清楚。我们使用全细胞膜片钳在解剖学上确定的第二阶压力感受器神经元在脑干切片测试是否组I，II和III mGluRs在这第一个中央突触的压力感受器传入通路的突触后效应。组I激动剂DHPG诱导的去极化和尖峰，是模仿内源性谷氨酸。I组mGluR阻断防止去极化和轻微超极化的神经元，这表明一个小的紧张性I组mGluR激活。DHPG诱导的内向电流由电压依赖性成分和非电压依赖性成分组成，前者可被TEA阻断，后者可被LiCl或Tris-HCl替代细胞外NaCl阻断。DHPG电流在无Ca ~（2+）的外部溶液中增强，用BAPTA进行细胞内透析和用Na ~+-Ca ~（2+）交换阻断剂KB-R7943或3′，4 ′-二氯苯扎明进行灌流可减弱DHPG电流。用GDPβS或肝素进行细胞内透析，并灌注PLC抑制剂U-73122或Ca ~（2+）-钙调蛋白抑制剂W-7，可显著降低DHPG电流。数据表明，压力感受器神经元上的I组mGluRs是功能性的;被内源性谷氨酸激活;并且通过G蛋白、PLC、IP 3和Ca 2 +-钙调蛋白机制激活Na+-Ca 2+交换器以兴奋细胞，从而提供突触后机制以增强或延长压力感受器信号传递。
The nucleus tractus solitarius (NTS) is essential for coordinating baroreflex control of blood pressure. The baroreceptor sensory fibers make glutamatergic synapses onto second-order NTS neurons. Glutamate spillover activates Group II and III presynaptic metabotropic glutamate receptors (mGluRs) on the baroreceptor central terminals to inhibit synaptic transmission, but the role of postsynaptic mGluRs is less understood. We used whole cell patch-clamping in anatomically identified second-order baroreceptor neurons in a brain stem slice to test whether Group I, II, and III mGluRs had postsynaptic effects at this first central synapse in the baroreceptor afferent pathway. The Group I agonist DHPG induced a depolarization and spiking that was mimicked by endogenous glutamate. Group I mGluR blockade prevented the depolarization and slightly hyperpolarized the neurons, suggesting a small tonic Group I mGluR activation. The DHPG-induced inward current consisted of voltage-dependent and -independent components; the former was blocked by TEA and the latter was blocked by replacing extracellular NaCl with LiCl or Tris-HCl. The DHPG current was potentiated in a Ca2+-free external solution and was diminished by intracellular dialysis with BAPTA and by perfusion with Na+–Ca2+exchanger blockers, KB-R7943 or 3′,4′-dichlorobenzamil. Intracellular dialysis with GDPβS or heparin and perfusion with the PLC inhibitor U-73122 or the Ca2+-calmodulin inhibitor W-7 significantly decreased the DHPG current. The data suggest that Group I mGluRs on baroreceptor neurons are functional; are activated by endogenous glutamate; and activate a Na+–Ca2+exchanger through G-protein, PLC, IP3, and Ca2+-calmodulin mechanisms to excite the cell, thus providing postsynaptic mechanisms to enhance or prolong baroreceptor signal transmission.