{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ramos DB"],"funding":["Fundação de Amparo à Pesquisa do Estado do Rio Grande do Sul (BR)","Conselho Nacional de Desenvolvimento Científico e Tecnológico (BR)","Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (BR)","Instituto Nacional de Ciência e Tecnologia para Excitotoxicidade e Neuroproteção","Financiadora de Estudos e Projetos (BR)"],"pagination":["149-59"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4749534"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(1)"],"pubmed_abstract":["In addition to its intracellular roles, the nucleoside guanosine (GUO) also has extracellular effects that identify it as a putative neuromodulator signaling molecule in the central nervous system. Indeed, GUO can modulate glutamatergic neurotransmission, and it can promote neuroprotective effects in animal models involving glutamate neurotoxicity, which is the case in brain ischemia. In the present study, we aimed to investigate a new in vivo GUO administration route (intranasal, IN) to determine putative improvement of GUO neuroprotective effects against an experimental model of permanent focal cerebral ischemia. Initially, we demonstrated that IN [(3)H] GUO administration reached the brain in a dose-dependent and saturable pattern in as few as 5 min, presenting a higher cerebrospinal GU"],"journal":["Purinergic signalling"],"pubmed_title":["Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats."],"pmcid":["PMC4749534"],"funding_grant_id":["IBN.Net 01.06.0842-00"],"pubmed_authors":["Dellavia GH","Ramos DB","Rocha GB","Almeida RF","Pettenuzzo LF","Hansel G","Muller GC","Souza DO","Horn AC","Ganzella M","Loureiro SO"],"additional_accession":[]},"is_claimable":false,"name":"Intranasal guanosine administration presents a wide therapeutic time window to reduce brain damage induced by permanent ischemia in rats.","description":"In addition to its intracellular roles, the nucleoside guanosine (GUO) also has extracellular effects that identify it as a putative neuromodulator signaling molecule in the central nervous system. Indeed, GUO can modulate glutamatergic neurotransmission, and it can promote neuroprotective effects in animal models involving glutamate neurotoxicity, which is the case in brain ischemia. In the present study, we aimed to investigate a new in vivo GUO administration route (intranasal, IN) to determine putative improvement of GUO neuroprotective effects against an experimental model of permanent focal cerebral ischemia. Initially, we demonstrated that IN [(3)H] GUO administration reached the brain in a dose-dependent and saturable pattern in as few as 5 min, presenting a higher cerebrospinal GU","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Mar","modification":"2025-04-25T19:01:26.034Z","creation":"2019-03-27T02:08:53Z"},"accession":"S-EPMC4749534","cross_references":{"pubmed":["26695181"],"doi":["10.1007/s11302-015-9489-9"]}}