This Article  • Full text  • PDF  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on ISI (1)  • Contact me when this article is cited  Related Content  • Similar articles in this journal

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

It has been known that the blockade of the N-methyl-D-aspartate receptor (NMDAR) induces a psychotomimetic state resembling schizophrenia. This clinical observation has led to developing the NMDAR hypofunction theory of schizophrenia, which states that the hypoglutamatergic state at postsynaptic NMDARs is involved in the pathophysiology of schizophrenia.¹ In a recent article, Anand et al² reported that lamotrigine, an agent inhibiting presynaptic glutamate release, attenuated the neuropsychiatric effects of ketamine, a noncompetitive NMDAR antagonist. In an attempt to explain the mechanism of action of lamotrigine, the authors hypothesized that ketamine may increase presynaptic glutamatergic release, producing a hyperglutamatergic state that enhances postsynaptic non–NMDAR-mediated glutamate transmission, and lamotrigine may attenuate the drug-induced effects by decreasing presynaptic glutamate release. Lamotrigine has been clinically tested to damp glutamate transmission in strokes, seizures, and cases of Alzheimer disease in which excessive glutamatergic transmission may be involved as a major pathophysiological mechanism.^3-5 However, in schizophrenia, . . . [Full Text of this Article]

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Is NMDA Receptor Hypofunction in Schizophrenia Associated With a Primary Hyperglutamatergic State?
Shim et al.
Arch Gen Psychiatry 2002;59:466-468.
FULL TEXT