Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury
Yang Gao, Siyi Xu, Zhenwen Cui, Mingkun Zhang, Yingying Lin, Lei Cai, Zhugang Wang, Xingguang Luo, Yan Zheng, Yong Wang, Qizhong Luo, Jiyao Jiang, Joseph H. Neale and Chunlong Zhong
Article first published online: 28 APR 2015 | DOI: 10.1111/jnc.13123
The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) suppresses glutamate transmission through selective activation of pre-synaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3) after traumatic brain injury (TBI). However, synaptically released NAAG is hydrolyzed to form N-acetylaspartate and glutamate mainly by Glutamate carboxypeptidase II (GCPII), losing neuroprotective effect. In this study, we found that knock out of the GCPII gene is not embryonic lethal and affords histopathological protection with improved long-term behavioral outcomes after TBI.