Whisker experience-dependent mGluR signaling maintains synaptic strength in the mouse adolescent cortex.
Whisker experience-dependent mGluR signaling maintains synaptic strength in the mouse adolescent cortex.
复制标题
晶须经验依赖性 mGluR 信号传导维持小鼠青少年皮层的突触强度。
DOI：
10.1111/ejn.13285
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发表时间：
2016
期刊：
影响因子：
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通讯作者：
M.
中科院分区：
文献类型：
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作者：
Kubota;J.;Mikami;Y.;Kanemaru;K.;Sekiya;H.;Okubo;Y. and Iino;M.
躯体感觉皮层中的感觉经验依赖性可塑性是适应不断变化的环境的基本机制，不仅在发育早期，而且在青春期和成年期。虽然在早期发育过程中经验依赖性可塑性的机制已经有了很好的记录，但对成熟皮层的相应理解还不完全。在这里，我们研究了胡须剥夺诱导的青春期小鼠桶皮质突触可塑性的机制。第4层（L4）至L2/3兴奋性突触对啮齿动物桶状皮质中的须经验依赖性可塑性起着至关重要的作用，并且已知须剥夺会抑制青少年和成年动物L4-L2/3突触的突触强度。我们发现，胡须剥夺5天或更长时间降低了突触前谷氨酸释放的概率在L4-L2/3突触的桶皮质在青春期小鼠。这种胡须剥夺诱导的抑郁症可以通过每天给予5型代谢型谷氨酸受体（mGluR 5）的正变构调节剂来恢复。另一方面，mGluR 5拮抗剂给药重现了胡须完整小鼠的胡须剥夺效应。此外，在突触后L2/3神经元中长期和选择性抑制肌醇1，4，5-三磷酸（IP 3）信号传导降低了L4-L2/3突触的突触前释放概率。这些发现代表了一种以前未确定的皮质可塑性机制，即突触后神经元中的须经验依赖性mGluR 5-IP 3信号传导维持青少年桶皮质的突触前功能。
Sensory experience‐dependent plasticity in the somatosensory cortex is a fundamental mechanism of adaptation to the changing environment not only early in the development but also in adolescence and adulthood. Although the mechanisms underlying experience‐dependent plasticity during early development have been well documented, the corresponding understanding in the mature cortex is less complete. Here, we investigated the mechanism underlying whisker deprivation‐induced synaptic plasticity in the barrel cortex in adolescent mice. Layer 4 (L4) to L2/3 excitatory synapses play a crucial role for whisker experience‐dependent plasticity in rodent barrel cortex and whisker deprivation is known to depress synaptic strength at L4–L2/3 synapses in adolescent and adult animals. We found that whisker deprivation for 5 days or longer decreased the presynaptic glutamate release probability at L4–L2/3 synapses in the barrel cortex in adolescent mice. This whisker deprivation‐induced depression was restored by daily administration of a positive allosteric modulator of the type 5 metabotropic glutamate receptor (mGluR5). On the other hand, the administration of mGluR5 antagonists reproduced the effect of whisker deprivation in whisker‐intact mice. Furthermore, chronic and selective suppression of inositol 1,4,5‐trisphosphate (IP3) signaling in postsynaptic L2/3 neurons decreased the presynaptic release probability at L4–L2/3 synapses. These findings represent a previously unidentified mechanism of cortical plasticity, namely that whisker experience‐dependent mGluR5‐IP3signaling in the postsynaptic neurons maintains presynaptic function in the adolescent barrel cortex.