| First Author | Karaca M | Year | 2014 |
| Journal | Neurochem Res | Volume | 39 |
| Issue | 3 | Pages | 456-9 |
| PubMed ID | 23595828 | Mgi Jnum | J:205028 |
| Mgi Id | MGI:5543887 | Doi | 10.1007/s11064-013-1041-0 |
| Citation | Karaca M, et al. (2014) Development of mice with brain-specific deletion of floxed glud1 (glutamate dehydrogenase 1) using cre recombinase driven by the nestin promoter. Neurochem Res 39(3):456-9 |
| abstractText | In the brain, Glud1-encoded glutamate dehydrogenase plays a major role in the recycling of the neurotransmitter glutamate. We recently reported a new model of brain-specific Glud1 null mice (Cns-Glud1 (-/-)) lacking glutamate dehydrogenase in the central nervous system. Cns-Glud1 (-/-) mice exhibit reduced astrocytic glutamate breakdown and redirection of glutamate pathways without altering synaptic transmission. Cns-Glud1 (-/-) mice were generated using LoxP and Nestin-Cre technology. Nestin-Cre mice are widely used to investigate gene deletion in the central nervous system. However, the Nes-Cre transgene itself was reported to induce a phenotype related to body weight gain. Here, we review the potential side-effects of Nes-Cre and analysed Cns-Glud1 (-/-) body weight gain. Overall, Nestin-Cre mice may exhibit transient and moderate growth retardation during the few weeks immediately following weaning. Pending appropriate controls and homogenization of the genetic background, Nestin-Cre technology is a valuable tool enabling disruption of genes of interest in the central nervous system. |
