Current-source density analysis in the rat olfactory bulb: Laminar distribution of kainate/AMPA- and NMDA-receptor-mediated currents
Current-source density analysis in the rat olfactory bulb: Laminar distribution of kainate/AMPA- and NMDA-receptor-mediated currents
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DOI：
10.1152/jn.1999.81.1.15
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发表时间：
1999-01-01
影响因子：
2.5
通讯作者：
Shipley, MT
中科院分区：
文献类型：
--
作者：
Aroniadou-Anderjaska, V;Ennis, M;Shipley, MT
采用一维电流源密度法分析刺激嗅神经（ON）层或二尖瓣细胞层（MCL）在大鼠嗅球切片中诱发的层流场电位分布，并识别场电位发生器和该网络中突触活动的特征。 ON 的单脉冲在肾小球层 (GL) 中引起延长的（大于或等于 400 ms）下沉 (S1(ON))，在外部丛状层 (EPL) 和 MCL 中产生相应的源，在 EPL 中引起相对短暂的下沉 (S2(ON))，在内部丛状层和颗粒细胞层中反转。这些汇/源分布表明 S1(ON) 和 S2(ON) 分别在二尖瓣/簇状细胞和颗粒细胞的顶端树突中产生。红藻氨酸/AMPA受体拮抗剂CNQX (10 μM)减少了S1(ON)的早期阶段，阻断了S2(ON)，并在EPL中的S2(ON)位置处显示了低振幅、延长的下沉。 CNQX 中 Mg2+ 的减少增强了 S1(ON) 的 CNQX 抗性成分和 EPL 汇。该 EPL 下沉反转至 MCL 以下，表明它是在颗粒细胞中产生的。 NMDA 受体拮抗剂 APV (50 μM) 可逆地阻断所有层中的 CNQX 抗性场电位。对 MCL 施加单脉冲，以逆向去极化二尖瓣/簇状细胞的树突。除了颗粒细胞的突触电流外，GL 中还引起低幅度、长时间的下沉 (S1(mcl))。相应的来源在 EPL 中，表明 S1(mcl) 是在二尖瓣/簇状细胞的肾小球树突簇中产生的。 S1(mcl) 和颗粒细胞电流几乎都被CNQX (10 μM) 阻断，但由于随后Mg2+ 的还原而增强，这些电流被APV 阻断。标准培养基中使用 γ-氨基丁酸-A-受体拮抗剂也能增强 S1(mcl)； APV 减少了这种增强。 ON 激活通过红藻氨酸/AMPA 和 NMDA 受体在二尖瓣/簇状细胞的顶端树突中产生长时间的兴奋，为嗅觉系统中突触处理第一级的感觉信息的调节和整合提供了机会。颗粒细胞通过红藻氨酸/AMPA 和 NMDA 受体对来自二尖瓣/簇状细胞侧树突的输入作出反应；然而，在细胞外 Mg2+ 的生理浓度下，NMDA 受体激活对颗粒细胞反应没有显着贡献。由二尖瓣/簇状细胞树突的逆向去极化引起的肾小球下沉表明，从二尖瓣/簇状细胞的顶端树突释放的谷氨酸可能会激发相同或邻近的二尖瓣/簇状细胞树突。
The one-dimensional current-source density method was used to analyze laminar field potential profiles evoked in rat olfactory bulb slices by stimulation in the olfactory nerve (ON) layer or mitral cell layer (MCL) and to identify the field potential generators and the characteristics of synaptic activity in this network. Single pulses to the ON evoked a prolonged (greater than or equal to 400 ms) sink (S1(ON)) in the glomerular layer (GL) with corresponding sources in the external plexiform layer (EPL) and MCL and a relatively brief sink (S2(ON)) in the EPL, reversing in the internal plexiform and granule cell layers. These sink/source distributions suggested that S1(ON) and S2(ON) were generated in the apical dendrites of mitral/tufted cells and granule cells, respectively. The kainate/AMPA-receptor antagonist CNQX (10 mu M) reduced the early phase of S1(ON), blocked S2(ON), and revealed a low amplitude, prolonged sink at the location of S2(ON) in the EPL. Reduction of Mg2+, in CNQX, enhanced both the CNQX-resistant component of S1(ON) and the EPL sink. This EPL sink reversed below the MCL, suggesting it was produced in granule cells. The NMDA-receptor antagonist APV (50 mu M) reversibly blocked the CNQX-resistant field potentials in all layers. Single pulses were applied to the MCL to antidromically depolarize the dendrites of mitral/tufted cells. In addition to synaptic currents of granule cells, a low-amplitude, prolonged sink (S1(mcl)) was evoked in the GL. Corresponding sources were in the EPL, suggesting that S1(mcl) was generated in the glomerular dendritic tufts of mitral/tufted cells. Both S1(mcl) and the granule cell currents were nearly blocked by CNQX (10 mu M) but enhanced by subsequent reduction of Mg2+ these currents were blocked by APV. S1(mcl) also was enhanced by gamma-aminobutyric acid-A-receptor antagonists applied to standard medium; this enhancement was reduced by APV. ON activation produces prolonged excitation in the apical dendrites of mitral/tufted cells, via kainate/AMPA and NMDA receptors, providing the opportunity for modulation and integration of sensory information at the first level of synaptic processing in the olfactory system. Granule cells respond to input from the lateral dendrites of mitral/tufted cells via both kainate/AMPA and NMDA receptors; however, in physiological concentrations of extracellular Mg2+, NMDA-receptor activation does not contribute significantly to the granule cell responses. The glomerular sink evoked by antidromic depolarization of mitral/tufted cell dendrites suggests that glutamate released from the apical dendrites of mitral/tufted cells may excite the same or neighboring mitral/tufted cell dendrites.