Title of article :
Alterations in cell adhesion molecule L1 and functionally related genes in major depression: A postmortem study
Author/Authors :
Daphna Laifenfeld، نويسنده , , Rachel Karry، نويسنده , , Ehud Klein، نويسنده , , Dorit Ben Shachar، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2005
Pages :
10
From page :
716
To page :
725
Abstract :
Background Current research in depression aims to delineate genes involved in neuronal plasticity that are altered in the disease or its treatment. We have shown antidepressant induced increases in three interrelated genes, cell adhesion molecule L1 (CAM-L1), laminin, and cAMP response element binding protein (CREB), and a reciprocal decrease in these genes consequent to stress. Presently we hypothesized that CAM-L1, CREB, and laminin may be altered in post mortem brains of depressed subjects. Methods Studies were performed in the prefrontal and in the ventral parieto-occipital cortices, of 59 brains from depressed, bipolar, and schizophrenic subjects, and normal controls, obtained from the Stanley Foundation Brain Collection. mRNA and protein levels were determined by RT-PCR and Western blot analysis, respectively. Results Levels of CAM-L1 and of phosphorylated CREB (pCREB) were increased in the prefrontal cortex of the depressed group, while CAM-L1, laminin and pCREB were decreased in the parieto-occipital cortex. Depressed subjects receiving antidepressants differed from subjects not receiving antidepressants in the expression of CAM-L1 and laminin in the parieto-occipital cortex, and in the expression of pCREB in the prefrontal cortex. Conclusions The present findings of specific alterations in depression and antidepressant treatment particularly in CAM-L1 suggest that this gene may play an important role in the pathophysiology and treatment of depression.
Keywords :
CREB , Antidepressant , depression , Laminin , plasticity , CAM-L1
Journal title :
Biological Psychiatry
Serial Year :
2005
Journal title :
Biological Psychiatry
Record number :
502611
Link To Document :
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