The kainic acid (KA)-induced status epilepticus model evoked in rats is commonly used in the search for both acutely anticonvulsant and disease-modifying therapies in both mice and rats. This model includes an acute status epilepticus insult that then is followed by a latent phase prior to the development of spontaneous recurrent seizures; e.g. epilepsy. While every model of a human disease evoked in an animal has its limitations, the KA model demonstrates the fidelity, pathophysiology, and pharmacological sensitivity to be consistent with clinical temporal lobe epilepsy.
In the categories essential to understanding the validity of an animal model of disease, the post KA-induced status epilepticus of temporal lobe epilepsy meets numerous desirable criteria:
- Face validity – i.e. the similarity of the model evoked in an animal model to the human condition.
- Construct validity – i.e. the ability of the model to accurately produce the outcome it is designed to reproduce.
- External validity – i.e. the generalizability of the model’s outcomes to other real-world scenarios.
As a valid preclinical model of both status epilepticus and acquired temporal lobe epilepsy, this model provides many benefits to apply to the early discovery of novel therapies. One of the more interesting findings that came out from an undergraduate student’s data mining project was the observation that body weight at the time of SE induction correlated, albeit modestly, to the subsequent burden of spontaneous recurrent seizures up to 6 weeks later.
Such a cool finding! These findings suggest that the larger the rat at the time of SE insult, the more likely he will be to develop a severe disease course much later post-SE onset.