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Sensitization Phenomena in Psychiatric Illness

Lessons from the Kindling Model

Received August 30, 1999; revised December 9, 1999; accepted December 21, 1999. From the Department of Psychiatry, University of North Carolina Neurosciences Hospital, CB;ns 7160, 101 Manning Drive, Chapel Hill, NC 27599–7160. Send correspondence to Dr. Kraus at the above address; e-mail: jkraus{at}med.unc.edu

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.

Key Words: Sensitization • Kindling • Schizophrenia • N-methyl-D-aspartate (NMDA)

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