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[P10]: IQGAP1 is a key protein in VEGF‐triggered neural progenitor cells migration
Author(s) -
Balenci L.,
Deloulme J.C.,
Saoudi Y.,
Bernards A.,
Baudier J.
Publication year - 2006
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2006.09.074
Subject(s) - key (lock) , progenitor cell , computer science , library science , medicine , biology , microbiology and biotechnology , stem cell , operating system
Depression is highly prevalent complex, heterogeneous disorder with possible serious physical, mental and socioeconomical consequences. There are several theories trying to explain the genesis of depression, one novel, links the depression with reduced brain plasticity. Neural cell adhesion (NCAM) plays important roles in the development of central nervous system and in the structural and functional plasticity in the CNS throughout life. NCAM is a member of the immunoglobulin superfamily of adhesion molecules is characterized by several immunoglobulin (Ig)-like domains. If the reduced neuronal plasticity is an important factor predisposing to the development of psychiatric disorders and depression in particular, than animals with reduced brain plasticity due to deficiency in NCAM should serve as a valuable model of depression. Mice (c56/BL strain) with genetic deficiency for NCAMs were subjected to two tests widely used for the assessment of depression-like phenotype: tails suspension test and sucrose preference test. NCAMdeficient mice demonstrated higher immobility time in the tail suspension test and lower preference for sucrose solution in sucrose consumption test as compared with their wild type littermates. The increased immobility time in tail suppression test was reversed by amitriptyline and citalopram treatment. Furthermore, a peptide with NCAMmimetic actions, FGL was also able to rescue “depression-like” phenotype in NCAM-deficient mice. Analysis of hippocampal neurogenesis in NCAMdeficient mice revealed a reduced survival and differentiation of the newly born cells into calbindinpositive granule neurons. At the same time point, larger proportion of young postmitotic neurons expressing Tuj1 was found in NCAM−/− mice. No changes in the proportion of BrdUpositive cells, which have been differentiated into glial phenotype, were found. In conclusion, NCAM-deficient mice demonstrate “depression-like” behaviour associated with reduced hippocampal neurogenesis and might serve as a genetic model of depression.