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.
Kraus
J E
JE
Department of Psychiatry, University of North Carolina Neurosciences Hospital, Chapel Hill 27599-7160, USA. jkraus@med.unc.edu
D004569:Electroencephalography; D004827:Epilepsy / Q000175:diagnosis* / Q000503:physiopathology / Q000523:psychology*; D006624:Hippocampus / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007696:Kindling, Neurologic / Q000502:physiology*; D001523:Mental Disorders / Q000175:diagnosis* / Q000209:etiology*; D010766:Phosphorylation; D017966:Pyramidal Cells / Q000378:metabolism; D017470:Receptors, Glutamate / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate