Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
Human chromosome 16p11.2 microdeletion is the most common gene copy number variation in autism, but the synaptic pathophysiology caused by this mutation is largely unknown. Using a mouse with the same genetic deficiency, we found that metabotropic glutamate receptor 5 (mGluR5)-dependent synaptic pla...
| প্রধান লেখক: | , , , , , , |
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| অন্যান্য লেখক: | |
| বিন্যাস: | প্রবন্ধ |
| ভাষা: | en_US |
| প্রকাশিত: |
Nature Publishing Group
2016
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| অনলাইন ব্যবহার করুন: | http://hdl.handle.net/1721.1/102336 https://orcid.org/0000-0001-6673-4988 |
| সংক্ষিপ্ত: | Human chromosome 16p11.2 microdeletion is the most common gene copy number variation in autism, but the synaptic pathophysiology caused by this mutation is largely unknown. Using a mouse with the same genetic deficiency, we found that metabotropic glutamate receptor 5 (mGluR5)-dependent synaptic plasticity and protein synthesis was altered in the hippocampus and that hippocampus-dependent memory was impaired. Notably, chronic treatment with a negative allosteric modulator of mGluR5 reversed the cognitive deficit. |
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