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首页> 外文期刊>The European Journal of Neuroscience >ZD7288 inhibits postsynaptic glutamate receptor-mediated responses at hippocampal perforant path-granule cell synapses.
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ZD7288 inhibits postsynaptic glutamate receptor-mediated responses at hippocampal perforant path-granule cell synapses.

机译：ZD7288抑制突触​​后谷氨酸受体介导的海马穿孔路径颗粒细胞突触的反应。

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摘要

Hyperpolarization-activated channels (Ih) are widely expressed in the nervous system and believed to play an important role in the regulation of membrane excitability and rhythmic activity. Recent evidence suggests that Ih may be involved in long-term potentiation (LTP) in the hippocampus; however, the results are controversial. To explore the possible causes of these differing results, the effects of Ih blockers on synaptic activity were evaluated in mouse hippocampal slices. ZD7288 (20 micro m), a selective Ih blocker, apparently prevented the induction of LTP, while Cs+ (1 mm), a commonly used Ih blocker, had no effect on LTP at hippocampal perforant path-dentate granule cell synapses. In addition, ZD7288 but not Cs+ abolished basal synaptic transmission. Results from voltage-clamp experiments showed that ZD7288 produced a very little inhibition on hyperpolarization-activated currents, indicating a weak expression of the Ih in granule neurons. Outside-out patch recordings revealed that ZD7288 inhibited glutamate receptor-mediated responses, while Cs+ had no effect on them. Meanwhile, ZD7288 reduced both alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate and N-methyl-d-aspartate receptor-mediated excitatory postsynaptic currents. The results suggest that ZD7288-induced reduction of synaptic transmission may result from its inhibition of the postsynaptic glutamate receptors on dentate granule neurons.
机译：超极化激活通道（Ih）在神经系统中广泛表达，并被认为在调节膜兴奋性和节律活动中起重要作用。最近的证据表明，Ih可能参与了海马的长期增强（LTP）。但是，结果是有争议的。为了探讨这些不同结果的可能原因，在小鼠海马切片中评估了Ih阻滞剂对突触活性的影响。选择性的Ih阻滞剂ZD7288（20微米）显然阻止了LTP的诱导，而常用的Ih阻滞剂Cs +（1毫米）对海马穿孔路径齿状颗粒细胞突触的LTP没有影响。此外，ZD7288而不是Cs +消除了基础突触传递。电压钳实验的结果表明，ZD7288对超极化激活电流几乎没有抑制作用，表明Ih在颗粒神经元中的表达较弱。从外而外的补丁录音表明ZD7288抑制了谷氨酸受体介导的反应，而Cs +对它们没有影响。同时，ZD7288减少了α-氨基-3-羟基-5-甲基异恶唑-4-丙酸酯和N-甲基-d-天冬氨酸受体介导的兴奋性突触后电流。结果表明，ZD7288诱导的突触传递减少可能是由于其抑制了齿状颗粒神经元上的突触后谷氨酸受体所致。

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