Jessié M Gutierres1, Fabiano B Carvalho2, Maria Rosa C Schetinger2, Patrícia Marisco2, Paula Agostinho3, Marília Rodrigues2, Maribel A Rubin2, Roberta Schmatz2, Cassia R da Silva2, Giana de P Cognato4, Julia G Farias2, Cristiane Signor2, Vera M Morsch2, Cinthia M Mazzanti2, Mauricio Bogo4, Carla D Bonan4, Roselia Spanevello5. 1. Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Av. Roraima, 97105-900 Santa Maria, RS, Brazil. Electronic address: jessiegutierres@hotmail.com. 2. Programa de Pós-Graduação em Bioquímica Toxicológica, Centro de Ciências Naturais e Exatas, Universidade Federal de Santa Maria, Av. Roraima, 97105-900 Santa Maria, RS, Brazil. 3. Center for Neuroscience and Cell Biology, Faculty of Medicine, University of Coimbra, Coimbra, Portugal. 4. Laboratório de Neuroquímica e Psicofarmacologia, Faculdade de Biociências, Pontifícia Universidade Católica do Rio Grande do Sul, Avenida Ipiranga, 6681, 90619-900 Porto Alegre, RS, Brazil. 5. Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário-Capão do Leão, 96010-900 Pelotas, RS, Brazil.
Abstract
AIMS: The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intracerebroventricular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na(+),K(+)-ATPase, Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT. MAIN METHODS: Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin+anthocyanin (STZ+ANT). After seven days of treatment with ANT (200mg/kg; oral), the rats were icv-STZ injected (3mg/kg), and four days later the behavior parameters were performed and the animals submitted to euthanasia. KEY FINDINGS: A memory deficit was found in the STZ group, but ANT treatment showed that it prevents this impairment of memory (P<0.05). Our results showed a higher anxiety in the icv-STZ group, but treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that the ANT treatment (100μM) tested displaces the specific binding of [(3)H] flunitrazepam to the benzodiazepinic site of GABAA receptors. AChE, Ca(+)-ATPase activities and NOx levels were found to be increased in HC and CC in the STZ group, which was attenuated by ANT (P<0.05). STZ decreased Na(+),K(+)-ATPase activity and ANT was able to prevent these effects (P<0.05). SIGNIFICANCE: In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT.
AIMS: The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intracerebroventricular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na(+),K(+)-ATPase, Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT. MAIN METHODS: Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin+anthocyanin (STZ+ANT). After seven days of treatment with ANT (200mg/kg; oral), the rats were icv-STZ injected (3mg/kg), and four days later the behavior parameters were performed and the animals submitted to euthanasia. KEY FINDINGS: A memory deficit was found in the STZ group, but ANT treatment showed that it prevents this impairment of memory (P<0.05). Our results showed a higher anxiety in the icv-STZ group, but treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that the ANT treatment (100μM) tested displaces the specific binding of [(3)H] flunitrazepam to the benzodiazepinic site of GABAA receptors. AChE, Ca(+)-ATPase activities and NOx levels were found to be increased in HC and CC in the STZ group, which was attenuated by ANT (P<0.05). STZ decreased Na(+),K(+)-ATPase activity and ANT was able to prevent these effects (P<0.05). SIGNIFICANCE: In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT.
Authors: Fabiano B Carvalho; Jessié M Gutierres; Andressa Bueno; Paula Agostinho; Adriana M Zago; Juliano Vieira; Pâmela Frühauf; José L Cechella; Cristina Wayne Nogueira; Sara M Oliveira; Caroline Rizzi; Roselia M Spanevello; Marta M F Duarte; Thiago Duarte; Odir A Dellagostin; Cinthia M Andrade Journal: Mol Neurobiol Date: 2016-05-11 Impact factor: 5.590
Authors: Francine R Ianiski; Catiane B Alves; Carla F Ferreira; Virginia C Rech; Lucielli Savegnago; Ethel A Wilhelm; Cristiane Luchese Journal: Metab Brain Dis Date: 2016-02-27 Impact factor: 3.584
Authors: Mariana F B Gerzson; Natália P Bona; Mayara S P Soares; Fernanda C Teixeira; Francine L Rahmeier; Fabiano B Carvalho; Marilda da Cruz Fernandes; Giovana Onzi; Guido Lenz; Relber A Gonçales; Roselia M Spanevello; Francieli M Stefanello Journal: Neurotox Res Date: 2020-01-29 Impact factor: 3.911