PMID- 24978930 OWN - NLM STAT- MEDLINE DCOM- 20150511 LR - 20140815 IS - 1098-2396 (Electronic) IS - 0887-4476 (Linking) VI - 68 IP - 10 DP - 2014 Oct TI - Evaluation of NCS-1, DARPP-32, and neurotrophins in hippocampus and prefrontal cortex in rats submitted to sepsis. PG - 474-9 LID - 10.1002/syn.21760 [doi] AB - Sepsis is defined as the host's reaction to infection and it is characterized by a systemic inflammatory response with important clinical implications. Central nervous system dysfunction secondary to sepsis is associated with local generation of pro- and anti-inflammatory cytokines, impaired cerebral microcirculation, disturbance of neurotransmitters, apoptosis, and cognitive impairment. It is known that during the process of learning and memory formation several pathways are involved such as dopaminergic and cholinergic systems. Thus, the objective of this study is to evaluate the neuronal calcium sensor (NCS-1) and dopamine-cAMP regulated phosphoprotein of 32,000 kDa (DARPP-32) expression as well as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) levels in prefrontal cortex and hippocampus of rats 12, 24, and 48 h after sepsis induction. To this aim, we used sham-operated Wistar rats or submitted to the cecal ligation and perforation procedure. After 12 and 24 h, there was an increase of NGF levels in hippocampus; and up to 48 h, a decrease of NCS-1 expression in prefrontal cortex, a decrease of BDNF levels in hippocampus and an increase of NGF levels in hippocampus. In conclusion, we believe that the low expression of NCS-1 in prefrontal cortex and low levels of BDNF in hippocampus may be associated with the pathophysiology of cognitive impairment during sepsis and a putative role of the dopaminergic system. CI - (c) 2014 Wiley Periodicals, Inc. FAU - Comim, Clarissa M AU - Comim CM AD - Postgraduate Program in Health Sciences, Laboratory of Experimental Neurosciences, Infectious Diseases Unit, University of South Santa Catarina, Palhoca, Santa Catarina, Brazil. FAU - Silva, Napoleao C AU - Silva NC FAU - Mina, Francielle AU - Mina F FAU - Dominguini, Diogo AU - Dominguini D FAU - Scaini, Giselli AU - Scaini G FAU - Morais, Meline O S AU - Morais MO FAU - Rosa, Daniela V AU - Rosa DV FAU - Magno, Luiz Alexandre V AU - Magno LA FAU - Streck, Emilio L AU - Streck EL FAU - Romano-Silva, Marco A AU - Romano-Silva MA FAU - Quevedo, Joao AU - Quevedo J FAU - Dal-Pizzol, Felipe AU - Dal-Pizzol F LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20140716 PL - United States TA - Synapse JT - Synapse (New York, N.Y.) JID - 8806914 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Dopamine and cAMP-Regulated Phosphoprotein 32) RN - 0 (Nerve Growth Factors) RN - 0 (Neuronal Calcium-Sensor Proteins) RN - 0 (Neuropeptides) RN - 0 (Ppp1r1b protein, rat) RN - 0 (frequenin calcium sensor proteins) RN - 9061-61-4 (Nerve Growth Factor) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/metabolism MH - Disease Models, Animal MH - Dopamine and cAMP-Regulated Phosphoprotein 32/*metabolism MH - Enzyme-Linked Immunosorbent Assay MH - Hippocampus/*metabolism MH - Immunoblotting MH - Male MH - Nerve Growth Factor/metabolism MH - Nerve Growth Factors/*metabolism MH - Neuronal Calcium-Sensor Proteins/*metabolism MH - Neuropeptides/*metabolism MH - Prefrontal Cortex/*metabolism MH - Rats, Wistar MH - Sepsis/*metabolism MH - Time Factors OTO - NOTNLM OT - BDNF OT - NGF OT - brain OT - cognitive impairment EDAT- 2014/07/01 06:00 MHDA- 2015/05/12 06:00 CRDT- 2014/07/01 06:00 PHST- 2014/03/31 00:00 [received] PHST- 2014/05/15 00:00 [revised] PHST- 2014/05/29 00:00 [accepted] PHST- 2014/07/01 06:00 [entrez] PHST- 2014/07/01 06:00 [pubmed] PHST- 2015/05/12 06:00 [medline] AID - 10.1002/syn.21760 [doi] PST - ppublish SO - Synapse. 2014 Oct;68(10):474-9. doi: 10.1002/syn.21760. Epub 2014 Jul 16.