Experimental analysis of behavior of Fyn-deficient mice

Fyn蛋白是Src家族的非受体型酪氨酸激酶之一，在大脑中强烈表达。观察fyn基因缺失小鼠对声源性听性癫痫的易感性，以及各种惊厥药物（包括mertrazol、picrotoxin、bicuculline、kainic acid、NMDA和士的宁）引起的癫痫的易感性。纯合子突变（fynz/fynz）小鼠更容易发生听原性癫痫发作。与杂合突变体（+/fynz）相比，给药时，他们更容易出现肌阵挛性惊厥，如美曲唑、微毒素、双曲霉素、kanic酸和NMDA。另一方面，纯合子突变体和杂合子突变体在服用士的宁时癫痫易感性没有差异。这些结果表明Fyn在由高声刺激和惊厥药物（抗gabaegic和谷氨酸/阿斯丁酸兴奋受体激动剂）引起的癫痫发作中起作用。

Fyn protein is one of the non-receptor type tyrosine kinases of the Src family and is strongly expressed in the brain. Mice deficient for the fyn gene were examined for their susceptibility to acoustically primed audiogenic seizures and seizures induced by various convulsive drugs, including mertrazol, picrotoxin, bicuculline, kainic acid, NMDA and strychnine. Homozygous mutant (fynz/fynz) mice were significantly more susceptible to audiogenic seizures. They were also more likely to show myoclonic convulsions than were heterozygous mutants (+/fynz) when metrazol, picrotoxin, bicuculline, kanic acid and NMDA were administered. On the other hand, no difference in seizure susceptibility was found between homozygous and heterozygous mutants when strychnine was administered. These results suggest a role of Fyn in seizures induced by loud acoustic stimulus and by convulsive drugs (anti-GABAeregic and glutamic/aspatic acid excitatory receptor agonists).