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Comparative genome- and proteome analysis of cerebral cortex from MK-801-treated rats.

Artikel i vetenskaplig tidskrift
Författare Linda Paulson
Peter Martin
Anders I. Persson
Carol L Nilsson
Elisabeth Ljung
Ann Brinkmalm-Westman
Peter S Eriksson
Kaj Blennow
Pia Davidsson
Publicerad i Journal of neuroscience research
Volym 71
Nummer/häfte 4
Sidor 526-33
ISSN 0360-4012
Publiceringsår 2003
Publicerad vid Institutionen för medicinsk och fysiologisk kemi
Institutionen för klinisk neurovetenskap
Sidor 526-33
Språk en
Länkar dx.doi.org/10.1002/jnr.10509
Ämnesord Animals, Cerebral Cortex, drug effects, metabolism, Dizocilpine Maleate, pharmacology, Gene Expression Regulation, drug effects, physiology, Genome, Oligonucleotide Array Sequence Analysis, methods, Proteome, drug effects, genetics, metabolism, RNA, Messenger, biosynthesis, Rats, Rats, Sprague-Dawley, Schizophrenia, genetics, metabolism
Ämneskategorier Neurobiologi

Sammanfattning

cDNA microarrays and two-dimensional gel-electrophoresis in combination with mass spectrometry, were used to screen alterations in mRNA and protein levels, respectively, in cerebral cortex of MK-801-treated rats. The rats were divided in two groups; group 1 (short-term treated) and group 2 (long-term treated). In group 1, four genes were up-regulated and five down-regulated. In group 2, seven genes were up-regulated and six down-regulated. In group 1, the levels of one protein was increased and eight proteins reduced. In group 2, the levels of two proteins were increased and four proteins reduced. Several of the altered genes (casein kinase 2, glutamic acid decarboxylase, synaptotagmin, gamma aminobutyric acid [GABA] transporter, creatine kinase, and cytochrome c oxidase) and proteins (superoxide dismutase, hsp 60, hsp 72 and gamma-enolase) have previously been connected to schizophrenia. Alterations of the genes (microglobulin, c-jun proto-oncogene, 40S ribosomal protein S19, adenosine diphosphate (ADP)-ribosylation factors, platelet-derived growth factor, fructose-bisphophate aldolase A, and myelin proteolipid) and the proteins (stathmin, H+-transp. Adenosine triphosphate (ATP) synthase, pyruvate dehydrogenase, beta-actin and alpha-enolase), have not, to our knowledge, earlier been implicated in schizophrenia pathology. Overall, these results with a combined approach of genomics and proteomics add to the validity of subchronic N-methyl-D-aspartate (NMDA)-receptor antagonist treatment as an animal model of schizophrenia.

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