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.
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.
Authors: A Schmitt; M Bauer; H Heinsen; W Feiden; P Falkai; I Alafuzoff; T Arzberger; S Al-Sarraj; J E Bell; N Bogdanovic; W Brück; H Budka; I Ferrer; G Giaccone; G G Kovacs; D Meyronet; M Palkovits; P Parchi; E Patsouris; R Ravid; R Reynolds; P Riederer; W Roggendorf; A Schwalber; D Seilhean; H Kretzschmar Journal: J Neural Transm (Vienna) Date: 2006-12-14 Impact factor: 3.575
Authors: Andrea Schmitt; Fernando Leonardi-Essmann; Pascal F Durrenberger; Sven P Wichert; Rainer Spanagel; Thomas Arzberger; Hans Kretzschmar; Mathias Zink; Mario Herrera-Marschitz; Richard Reynolds; Moritz J Rossner; Peter Falkai; Peter J Gebicke-Haerter Journal: Eur Arch Psychiatry Clin Neurosci Date: 2012-03-23 Impact factor: 5.270