By the systemic (i.p., s.c., or i.v.) or local intracerebral injection of kainic acid (KA) into different regions of the brain of experimental animals, status epilepticus and brain damage are induced. After a latent period, progressive neuronal loss, axon sprouting and rewiring, and spontaneously recurrent seizures occurred, which are similar to the pathogenesis of the human temporal lobe epilepsy. Hence, KA models have been considered to be suitable for clarifying the mechanism of onsets of spontaneously recurrent seizures in human and for evaluating or screening anti-epileptic drugs. In this paper, we will review different seizure models induced by KA and its relevant neuropathological changes, discuss possible mechanisms for seizure generation and summarize current therapeutic approaches to control seizures and neuropathological changes. Hopefully, it will shed light on better understanding the mechanism of epiletogenesis in patients with temporal lobe epilepsy, and provide some clues for the development of novel therapeutic approaches to effectively control human intractable epilepsy.