Kindling is an experimental model of epilepsy that involves activity-d
ependent changes in neuronal structure and function. During kindling,
pathological changes may occur at several organizational levels of the
nervous system, from alterations in gene-expression in individual neu
rons to the loss of specific neuronal populations and rearrangement of
synaptic connectivity resulting from sustained stimulation of major e
xcitatory pathways. This review summarizes recent developments in alte
rations at single neuronal and molecular levels that may be responsibl
e for kindling epileptogenesis.