Experimental analysis of behavior of Fyn-deficient mice

Fyn蛋白是Src家族中的一种非受体型酪氨酸激酶，在大脑中强烈表达。检测了fyn基因缺陷小鼠对听觉刺激的听源性癫痫的敏感性，以及由各种惊厥药物诱发的癫痫发作，这些药物包括硫唑、印防己毒素、荷包牡丹碱、海人藻酸、NMDA和士的宁。纯合子突变(fynz/fynz)小鼠明显更容易发生听源性癫痫。当使用美曲唑、印防己毒素、荷包牡丹碱、卡尼酸和NMDA时，他们也比杂合子突变体(+/fynz)更容易出现肌阵挛发作。另一方面，用用士的宁后，纯合子突变体和杂合突变体之间的癫痫敏感性没有发现差异。这些结果表明，Fyn在强声刺激和惊厥药物(抗GABA和谷氨酸/天冬氨酸兴奋性受体激动剂)诱导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).