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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs

Life Sci. 2002 Apr 19;70(22):2699-705.
Decreased density of [3H]TCP binding following antipsychotic drug withdrawal in rats.

Scarr E, Parkin FM, Pavey G, Dean B.

The Molecular Schizophrenia Division, The Mental Health Research Institute of Victoria, Parkville, Australia.

Antipsychotic drugs have been reported to increase the expression of subunits of the NMDA receptor at the level of mRNA but it is not clear whether such effects are apparent at the level of the radioligand binding or receptor protein. Therefore, we examined the effect of treatment of, and withdrawal from, haloperidol, chlorpromazine, olanzapine or clozapine on the binding of [3H]N-[1-(2-thienyl)cyclohexyl]piperidine ([3H]TCP ) to the open ion channel of the NMDA receptor in rat caudate-putamen, hippocampus and frontal cortex. [3H]TCP binding was not significantly different in the caudate-putamen, hippocampus and cortex after three months of treatment with any antipsychotic drug. There were significant decreases in [3H]TCP binding in rat caudate-putamen and cortex, but not hippocampus, one month after ceasing treatment. Decreases in the caudate-putamen were detected in rats previously treated with chlorpromazine (0.1 mg/kg/day) and clozapine (0.1 and 1.0 mg/kg/day). In the cortex, decreases in [3H]TCP binding were also detected in rats previously treated with olanzapine (0.1 mg/kg/day) for three months. These data suggest that changes in the NMDA receptor associated ion channels occur following antipsychotic drug withdrawal.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12269396&dopt=Abstract

Brain Res. 2002 Oct 4;951(2):166-76.
Alterations in regional brain metabolism in genetic and pharmacological models of reduced NMDA receptor function.

Duncan G, Miyamoto S, Gu H, Lieberman J, Koller B, Snouwaert J.

Department of Psychiatry, CB #7090, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7090, USA. gduncaed.unc.edu

A mouse line has been developed that expresses low levels of the NMDA R1 (NR1) subunit of the NMDA receptor [Cell 98 (1999) 427]. These NR1 hypomorphic mice represent an experimental model of reduced NMDA receptor function that may be relevant to the pathophysiology of schizophrenia. To further characterize the neurobiological phenotype resulting from developmental NMDA receptor hypofunction, regional brain metabolic activity was assessed by autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake. In addition, ligand binding to NMDA, AMPA, and kainate receptors was measured by quantitative autoradiography. MK-801 binding to NMDA receptors was reduced markedly throughout the brain of the NR1 hypomorphic mice. However, no alteration in 3H-AMPA or 3H-kainate binding was apparent in any region examined. Neuroanatomically specific alterations in regional 2-DG uptake were observed in the NR1 hypomorphic animals. Reduced relative 2-DG uptake was observed in the medial prefrontal and anterior cingulate cortices. Altered patterns of 2-DG uptake were also found in neocortical regions, with selective reductions of uptake in layer 6 in frontal regions of somatosensory and motor cortices. These data indicate alterations in cortical circuitry in the NR1 hypomorphic animals and are consistent with functional imaging studies in chronic schizophrenia patients which typically show reduced frontal cortical metabolic activity. Reduced relative 2-DG uptake was also found in the caudate, accumbens, hippocampus, and select thalamic regions in the NR1-deficient mice. However, in many other brain regions no alteration in 2-DG uptake was observed. The alterations in 2-DG uptake in the NR1 hypomorphic mice were distinctly different compared to those observed after acute challenge with the selective NMDA antagonist MK-801 in wild-type mice. The altered patterns of brain 2-DG uptake in the NR1 hypomorphic mice found in the present work, together with the altered behavioral phenotypes previously described, suggest that the mice may provide a valuable model to study novel therapeutic strategies to counteract the neurobiological consequences of chronic developmental NMDA receptor hypofunction.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12270494&dopt=Abstract

Neurosci Lett. 2002 Sep 27;330(3):290-2.
No association between a transcription factor Activating Protein 2beta (AP-2beta) gene variant and schizophrenia.

Jonsson EG, Damberg M, Forslund K, Mattila-Evenden M, Rylander G, Asberg M, Oreland L, Sedvall GC.

Department of Clinical Neuroscience, HUBIN project, Psychiatry Section, Karolinska Institute and Hospital, SE-171 76 Stockholm, Sweden. eriks.se

Genetic components are involved in the aetiology of schizophrenia. Activating Protein 2 (AP-2) transcription factors are essential for neural gene expression and neural development. Transcription factor AP-2beta has also been connected with monoaminergic genes and monoamine levels in various brain regions. Thus, the AP-2beta gene is a suitable candidate taking both the neurodevelopmental and dopamine hypotheses of schizophrenia into account. We investigated 135 schizophrenic patients and 382 control subjects with regard to an intronic AP-2beta variant without evidence of any association. We conclude that the investigated AP-2beta variant is not of major importance to schizophrenia in the investigated Swedish population. 2002 Elsevier Science Ltd.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12270648&dopt=Abstract

Adolesc Med. 2002 Oct;13(3):643-62.
The role of neuropsychological testing and evaluation: when to refer.

Banks ME.

This article examines neuropsychological deficits associated with several medical disorders (HIV infection, sickle cell disease, diabetes, and Turner syndrome), psychiatric disorders (schizophrenia, conduct disorder, mood disorder, and substance abuse disorder), and traumatic brain injury, especially as a consequence of child and relationship abuse. The literature reviewed includes attention to developmental and sociocultural considerations (gender, ethnicity, interpersonal violence, family function). A brief overview of changes in neuropsychological practice is provided. The focus of the article is on the use of neuropsychological evaluation as a first step in rehabilitation for adolescents with neuropsychological deficits. A complex clinical case evaluated with the Ackerman-Banks Neuropsychological Rehabilitation Battery is included to demonstrate the way in which identification of neuropsychological strengths and weaknesses can be used to develop treatment recommendations.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12270805&dopt=Abstract [PubMed - in process]

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