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Results: 1 to 3 of 3

Publication Record


Identity crisis involving body image in a young man with autism.
Warren ZE, Sanders KB, Veenstra-VanderWeele J
(2010) Am J Psychiatry 167: 1299-303
MeSH Terms: Adolescent, Anticonvulsants, Anxiety Disorders, Autistic Disorder, Behavior Therapy, Body Dysmorphic Disorders, Body Image, Child, Combined Modality Therapy, Cycloserine, Depressive Disorder, Major, Follow-Up Studies, Humans, Identity Crisis, Lamotrigine, Patient Care Team, Psychotherapy, Psychotropic Drugs, Socialization, Triazines, Young Adult
Added January 20, 2015
0 Communities
1 Members
0 Resources
21 MeSH Terms
Intracellular modulation of NMDA receptor function by antipsychotic drugs.
Leveque JC, MacĂ­as W, Rajadhyaksha A, Carlson RR, Barczak A, Kang S, Li XM, Coyle JT, Huganir RL, Heckers S, Konradi C
(2000) J Neurosci 20: 4011-20
MeSH Terms: Animals, Antipsychotic Agents, Blotting, Northern, Cells, Cultured, Clozapine, Cycloserine, Dizocilpine Maleate, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Gene Expression Regulation, Genes, fos, Haloperidol, Male, Neostriatum, Neurons, Phosphorylation, Rats, Rats, Sprague-Dawley, Receptors, N-Methyl-D-Aspartate, Signal Transduction
Show Abstract · Added May 27, 2014
The present study deals with the functional interaction of antipsychotic drugs and NMDA receptors. We show that both the conventional antipsychotic drug haloperidol and the atypical antipsychotic drug clozapine mediate gene expression via intracellular regulation of NMDA receptors, albeit to different extents. Data obtained in primary striatal culture demonstrate that the intraneuronal signal transduction pathway activated by haloperidol, the cAMP pathway, leads to phosphorylation of the NR1 subtype of the NMDA receptor at (897)Ser. Haloperidol treatment is likewise shown to increase (897)Ser-NR1 phosphorylation in rats in vivo. Mutation of (896)Ser and (897)Ser to alanine, which prevents phosphorylation at both sites, inhibits cAMP-mediated gene expression. We conclude that antipsychotic drugs have the ability to modulate NMDA receptor function by an intraneuronal signal transduction mechanism. This facilitation of NMDA activity is necessary for antipsychotic drug-mediated gene expression and may contribute to the therapeutic benefits as well as side effects of antipsychotic drug treatment.
0 Communities
1 Members
0 Resources
20 MeSH Terms
L-cycloserine slows the clinical and pathological course in mice with globoid cell leukodystrophy (twitcher mice).
LeVine SM, Pedchenko TV, Bronshteyn IG, Pinson DM
(2000) J Neurosci Res 60: 231-6
MeSH Terms: Animals, Brain, Cycloserine, Leukodystrophy, Globoid Cell, Mice, Mice, Mutant Strains
Show Abstract · Added March 5, 2014
Globoid cell leukodystrophy (Krabbe's disease) is an autosomal recessive disease that affects the lysosomal enzyme galactosylceramidase. Galactosylceramidase removes galactose from galactosylceramide and psychosine, which are derived from sphingosine. In the present study, L-cycloserine (an inhibitor of 3-ketodyhydrosphingosine synthase) was administered to the twitcher mouse, an authentic model of globoid cell leukodystrophy. Twitcher mice treated with L-cycloserine had a significantly longer life span and a delayed onset of weight loss than vehicle-injected twitcher mice. Pathological features such as macrophage infiltration and astrocyte gliosis also were less in treated twitcher mice. These results indicate that substrate reduction therapy may have therapeutic value for individuals with residual enzymatic activity, e.g., individuals with late onset disease or individuals with partial enzyme replacement via bone marrow transplantation. In these cases, a reduction in galactosylceramide and psychosine synthesis would enable residual enzymatic activity to keep up with the accumulation of these substrates that would otherwise lead to pathology.
Copyright 2000 Wiley-Liss, Inc.
0 Communities
1 Members
0 Resources
6 MeSH Terms