Development of Mice with Brain-Specific Deletion of Floxed Glud1 (Glutamate Dehydrogenase 1) Using Cre Recombinase Driven by the Nestin Promoter |
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Authors: | Melis Karaca Pierre Maechler |
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Affiliation: | 1. Department of Cell Physiology and Metabolism, University of Geneva Medical Centre, 1 rue Michel-Servet, 1211, Geneva 4, Switzerland
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Abstract: | 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. |
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