Epilepsy is a disease characterized by "paroxysmal, hypersynchronous, and excessive electrical discharges". Despite long and extensive research on epileptogenesis, clear explanation of the basic mechanisms of epilepsy has yet to be established. Considering the diverse etiologies of epilepsy and experimental seizure models, a seizure has many mecha-nisms affecting single neurons and its neural circuits. Epileptic neuron has the ability of spontaneous depolarization and firing. To achieve depolarization, these neurons tend to have increased membrane excitability by interaction of neuro-transmitter receptors and ion channels and synapses, but excitable single neuron does not necessarily mean hyperex-citable neural circuit. Synchrony, burst, and neural interactions are required for the spreading of the electrical dis-charges. Increased membrane excitability is mainly achieved by increased influx of calcium and decreased potassium and chloride transport mechanism. With this membrane excitability, paroxysmal depolarization shift (PDS) needs synaptic excitation represented by giant EPSP. Synaptic function is mainly controlled by neurotransmitters such as GABA and glutamate. The imbalance of these important neurotransmitters has a crucial role in epilepsy. Synaptic reor-ganization and associated change of neurotransmitter plays an essential role in chronic epileptogenesis.