Figure [1]: This diagram shows the classification of many animal epilepsy models, including Generalised Tonic-Clonic Seizure (GTCS), Absence Seizure, Myoclonus, and Status Epilepticus models, along with their subtypes.
Animal models of epilepsy or seizures in the research and development of ASMs,
Studying epilepsy and epileptic convulsions using in vitro preparations is worthwhile and practical. From practically any species, these preparations can be obtained [19] . Mammalian brain slices are the method that researchers employ the most frequently when looking at epileptiform activity. These thin brain slices can either be employed immediately (the acute brain slice preparation) or after being preserved in culture for several days or weeks in an incubator (the organotypic brain slice preparation) [20] .
Brain preparations from various mammalian species, including rabbits, guinea pigs, rats, mice, and humans after neurosurgical resections, have induced in vitro epileptiform activity [21] . The most often used species has been rats, and several strains have been used. However, the appeal of using mouse models for experiments has grown due to the relatively simple process of altering the mouse genome and the recent widespread usage of transgenic mouse strains. Differing mouse strains exhibit differing sensitivity to epileptogenic circumstances or might have developmental flaws or other traits due to their varied genetic backgrounds. Rats and other rodent species behave similarly[22] .
The age of the animal from which brain tissue is obtained significantly impacts the appearance of epileptiform activity in vitro[23] . However, it is unclear how an animal’s age affects how easily they can induce seizure-like episodes in vitro[24] . For instance, using the high K+ model, seizure-like events are not elicited in tissue from animals younger than postnatal day 5 (P5) in rat hippocampus slices. These are easiest to evoke at P12 before becoming challenging to create in animal tissue beyond P21[23] . Age-related variations in excitability and seizure propensity are controlled by several different processes, which leads to such complexity. As one illustration, GABAergic signaling is hypothesized to depolarize early in development compared to adult tissue because of high amounts of intracellular chloride [25] . Remembering that different species, strains, and sexes have varied maturational trajectories and alterations in various signaling pathways is crucial. At P7–P12, Rat and mouse pups are compared to newborn humans in terms of development. Experimental groups have to be appropriately randomized for the ages of the animals, and the impact of age is correctly accounted for in study statistics and reported in published manuscripts [26] .
In Vivo Models
To elucidate the neurochemical, neurophysiological, cellular, and molecular mechanisms that control epileptic seizures, several experimental models have been created in which epileptic activity is replicated and various treatments are explored. Studies on these models have also helped search for pathways similar to those that cause real epilepsy. The various animal models can be grouped into convulsively induced chemically, such as penicillin and cobalt, electrically, such as kindling and electroshock, or genetically, such as audiogenic seizures[27] . Scientists and researchers work to understand the mysteries of life and the intricacies of diseases and to create novel remedies in the field of biomedical research. In vivo models, which bridge the gap between in vitro experiments and clinical trials, are crucial in this endeavor. In vivo models frequently involve living things and provide unique benefits for examining biological processes, disease mechanisms, and prospective therapeutic approaches.
Although these models have tried to explain the underlying mechanics of this condition precisely, the cause of the development of so many distinct varieties of epilepsy has not yet been identified. Partial epilepsy, tonic-clonic convulsions, and status epilepticus (SE) were the three categories Fisher proposed for an epileptogenic classification of models in 1989. This review comprises the most prevalent in vivo epileptogenesis models currently understood by this classification. Fisher’s classification of epilepsy models, as modified for this review, only refers to in vivo models [28] . See Figure 1.