Flash photolysis reveals a diversity of ionotropic glutamate receptors on the mitral cell somatodendritic membrane.
Flash photolysis reveals a diversity of ionotropic glutamate receptors on the mitral cell somatodendritic membrane.
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闪光光解揭示了二尖瓣细胞体树突膜上离子型谷氨酸受体的多样性。
DOI：
10.1152/jn.00180.2003
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发表时间：
2003
期刊：
影响因子：
--
通讯作者：
Lowe,Graeme
中科院分区：
文献类型：
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作者：
Lowe,Graeme
人们普遍认为嗅球僧帽细胞的索马和基底树突只接受来自局部中间神经元的抑制性突触输入。然而，二尖瓣体树突膜表现出多种谷氨酸受体的免疫反应性，并阻断GABA受体揭露二尖瓣细胞的自我兴奋。这种兴奋被认为是由二尖瓣细胞自身释放的谷氨酸的扩散溢出或谷氨酸释放颗粒细胞的点状传输介导的。本研究通过硝基吲哚啉笼状谷氨酸盐的闪光光解检查了二尖瓣细胞谷氨酸盐敏感性的药理学和动力学，这有助于突触间隙中受体的可靠激活。将约0.5-1 mM谷氨酸盐释放到索马上的宽场激光（3.5-ms闪光）激活具有快速（3.4-ms上升，7.5-ms衰减）和慢速（64-ms上升，>10-s衰减）组分的大电流。在100 μM APV中，慢电流降低至对照的53%（257 ms上升，2 s衰减），在1.3 mM Mg 2+中显示外向整流，并被15 μM 5，7-二氯犬尿酸阻断。100 μM APV完全拮抗100 μM谷氨酸的反应，与高亲和力NMDA受体的竞争性抑制一致。没有观察到抗APV的NMDA受体，反驳了点状传播模型。快电流被10 μM NBQX阻断，被100 μM环噻嗪增强3.28倍，并被100 μM SYM 2206分解为AMPA（40%）和红藻氨酸（60%）受体组分。结果表明，自激依赖于AMPA，红藻氨酸，和传统的NMDA受体的二尖瓣细胞。
It is widely held that the soma and basal dendrites of olfactory bulb mitral cells receive exclusively inhibitory synaptic input from local interneurons. However, the mitral somatodendritic membrane exhibits immunoreactivity for a variety of glutamate receptors, and blocking GABA receptors unmasks mitral cell self-excitation. This excitation is proposed to be mediated either by diffuse spillover of the mitral cells' own released glutamate, or by punctate transmission from glutamate-releasing granule cells. This study examined the pharmacology and kinetics of glutamate sensitivity of mitral cells by flash photolysis of nitroindoline caged glutamates, which facilitate reliable activation of receptors in the synaptic cleft. Wide-field laser uncaging (3.5-ms flash) of approximately 0.5–1 mM glutamate onto the soma activated large currents with fast (3.4-ms rise, 7.5-ms decay) and slow (64-ms rise, >10-s decay) components. In 100 μM APV, slow currents were reduced to 53% of control (257-ms rise, 2-s decay), displayed outward rectification in 1.3 mM Mg2+, and blocked by 15 μM 5,7-dichlorokynurenate. Responses to ≲100 μM glutamate were fully antagonized by 100 μM APV, consistent with competitive inhibition at high-affinity NMDA receptors. An APV-resistant NMDA receptor was not observed, refuting the punctate transmission model. Fast currents were blocked by 10 μM NBQX, boosted 3.28-fold by 100 μM cyclothiazide, and resolved into AMPA (40%) and kainate (60%) receptor components by 100 μM SYM2206. The results suggest that self-excitation depends on AMPA, kainite, and conventional NMDA autoreceptors on the mitral cell.