This AOP begins with the interaction of chemicals to the picrotoxin binding site of the ionotropic GABA receptor complex causing blockage of the ion channel. As a result, decrease in inward chloride conductance occurs, followed by a reduction in postsynaptic inhibition, reflected as reduced frequency and amplitude of spontaneous inhibitory postsynaptic current or abolishment of GABA-induced firing action. Consequently, the resistance of excitatory neurons to fire is decreased, resulting in the generation of a large excitatory postsynaptic potential (EPSP) that causes voltage-gated Na⁺ to open, which results in action potentials. The depolarisation is followed by a period of hyper-polarisation mediated by Ca²⁺-dependent K⁺ channels or GABA-activated Cl⁻ influx, which becomes smaller, gradually disappears, and is replaced by a depolarisation known as “paroxysmal depolarizing shift” (PDS). A PDS is an indication of epilepsy at the cellular level and initiates the adverse outcome at the organismal level of epileptic seizure.