Sensitization phenomena in psychiatric illness: lessons from the kindling model

Sensitization or "kindling-like" phenomena have been implicated in the pathophysiology of a number of psychiatric illnesses. A basic understanding of the prototypical sensitization phenomenon, the kindling model of epilepsy, is thus of increasing significance for the psychiatrist. This article presents a summary of the kindling model, with particular emphasis on glutamatergic mechanisms in general and plasticity of the N-methyl-D-aspartate (NMDA) receptor in specific. Findings from the kindling model are then discussed in light of their potential relevance to psychiatric illness. Finally, a speculative model is proposed in which opposing molecular processes lead to NMDA receptor hyperfunction in kindling and hypofunction in schizophrenia.