动物造模,转基因动物模型 z-bio 2021-04-01 266

　　(1) Progressive myoclonic epilepsy syndrome model, namely cystatin B gene knockout mouse model. The Cystatin B gene encodes Cystatin B, a Cystatin protein kinase inhibitor. If the gene is knocked out, cystatin B cannot be expressed. Patients with U-LPME have mutations in this gene and lose function. Cystatin knockout mice and U-L PME patients have a special overlap in neurophenotype.

　　(2) Shaker-type delayed rectifier potassium channel gene knockout mouse model A gene knockout model based on K + channel block design can cause epilepsy. This type of animal may suffer from a severe nourishing clonal attack, leading to premature death.

　　(3) Rats with high-pressure active Ca2 + channel subunit gene aA subunit mutant; β4 subunit mutant sleepy mice; γ2 subunit mutant stargazers altered the epilepsy model of mice. Mutations in these subunit genes increase the excitability of rat brain neuron membranes, making them more susceptible to epilepsy.

　　(4) Transgenic Q54 mouse model Q54 mice have seizures starting at 2 months old, with restricted behavior and slow repetitive movements. Continuous EEG monitoring showed that seizure activity in the hippocampus was restricted and extended to the cortex. Pathological examination revealed a large number of cell loss and gliosis in hippocampal CA1-3 and hilar area. Transgenic Q54 mice provide a genetic model in which SCN2A is known to be a candidate gene for human epilepsy.

　　The advantage of gene knockout and transgenic epilepsy models is that they can study the interaction of epilepsy-related genes that are not available in other types of models, but the expression of each gene is related to its genetic background. Many literatures also point out that knockout or transplantation The genes have different phenotypes under different vector gene backgrounds. Therefore, researchers need to consider these influencing factors when evaluating experimental data.