NMDA 受体激动剂未能改变小脑篮状细胞的递质释放。
NMDA receptor agonists fail to alter release from cerebellar basket cells.
机构信息
Vollum Institute, Oregon Health & Science University, Portland, Oregon 97239, USA.
出版信息
J Neurosci. 2011 Nov 16;31(46):16550-5. doi: 10.1523/JNEUROSCI.3910-11.2011.
Abstract
Previous studies of NMDA receptor (NMDAR) expression on axons of cerebellar molecular layer interneurons have produced conflicting results. We made use of the calcium sensitivity of vesicular release machinery to test for NMDAR activity in basket cell axons. Iontophoresis of l-aspartate, an NMDAR agonist, onto basket cell axon collaterals had no effect on evoked IPSCs measured in synaptically coupled Purkinje cells. Furthermore, calcium indicators in basket cell varicosities did not report any change in intracellular calcium following iontophoresis of l-aspartate or two-photon uncaging of glutamate. In contrast, activation of presynaptic purinergic receptors by iontophoresis of ATP decreased evoked IPSC amplitudes and action potential-evoked calcium transients in axonal varicosities, demonstrating the effectiveness of activating presynaptic receptors by iontophoresis. We find no evidence for functional NMDARs in basket cell varicosities.
摘要
先前关于小脑分子层中间神经元轴突上 NMDA 受体（NMDAR）表达的研究得出了相互矛盾的结果。我们利用囊泡释放机制的钙敏感性来检测篮状细胞轴突中的 NMDAR 活性。将 NMDAR 激动剂 L-天冬氨酸离子导入到篮状细胞轴突侧支上，对突触偶联的浦肯野细胞中测量到的诱发 IPSC 没有影响。此外，篮状细胞末梢中的钙指示剂在注入 L-天冬氨酸或双光子解笼谷氨酸后，没有报告细胞内钙有任何变化。相比之下，通过离子导入 ATP 激活突触前嘌呤能受体，可降低轴突末梢中诱发 IPSC 幅度和动作电位诱发的钙瞬变，表明通过离子导入激活突触前受体的有效性。我们没有发现篮状细胞末梢中功能性 NMDAR 的证据。
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