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Título:
EVALUATION OF GENES IMPLICATED IN NEURONAL PLASTICITY AS POTENTIAL PERIPHERAL MARKERS OF COGNITIVE DEFICIT.
Autor/es:
ALEJANDRO DAVID MORONI; ANA MARÍA GENARO; MARÍA LAURA PALUMBO
Lugar:
Buenos Aires
Reunión:
Congreso; REUNIÓN CONJUNTA DE SOCIEDADES DE BIOCIENCIAS; 2017
Institución organizadora:
SAIC, SAIB, SAI, SAA, SAB, SAB, SAFE, SAFIS, SAH, SAP
Resumen:
The hippocampus is a brain-structure related with learningand memory. Hippocampus is sensitive to the stress effects. Inprevious reports, we found that chronic mild stress (CMS) model inducedcognitive deficit in mice. This was correlated with a decreasein adult neurogenesis and Th1/Th2 balance in lymphocytes. Wealso observed a decrease in neural nitric oxide synthase (nNOS)activity and protein levels and an increase in endothelial nitric oxidesynthase (eNOS) in hippocampus of CMS mice. Moreover,other authors related the genes G protein subunit alpha q (GNAQ),cAMP responsive element binding protein (CREB) and glycogensynthase kinase 3 beta (GSK-3b) with plasticity neuronal processsuch as neurogenesis, neuronal differentiation, dendritic growth andin several psychiatric disorders. All these genes are expressed inlymphocytes. The aim of the present work was correlate the eNOS,nNOS, GNAQ, CREB and GSK-3b genes expression in hippocampus,lymph nodes and spleen with cognitive deficit in female BALB/cmice exposed to CMS model. The spontaneous alternation percentagewas evaluated by Y-maze. We found a poor performance in theY-maze in CMS mice respect to control mice (p<0.01). The mRNAlevels of the all genes were analyzed by qRT-PCR. The mRNA levelof eNOS (p<0.05), nNOS (p<0.05) and GNAQ (p<0.05) decreasein hippocampus and nNOS (p<0.05) level decease in lymph nodesof stressed mice respect to control. The GNAQ (p<0.05), GSK-3b(p<0.01) and CREB (p<0.01) expression decrease in spleen of CMSmice. The other genes did not show significant differences in thestudied tissues. These findings indicate the nNOS and GNAQ genescould be potential peripheral markers of cognitive deficit.