Journal
FRONTIERS IN PSYCHIATRY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fpsyt.2021.701408
Keywords
major depressive disorder; psychopharmacology; purines (source: MeSH); guanosine; purinergic signaling; olfactory bulbectomy
Categories
Funding
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES)
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq)
- Instituto Nacional de Ciencia e Tecnologia (INCT) para Excitotoxicidade e Neuroprotecao
- Fundacao de Amparo a Pesquisa do Estado do Rio Grande do Sul (FAPERGS)
- Financiadora de Estudos e Projetos (FINEP) research grant Rede Instituto Brasileiro de Neurociencias (IBNNet) [01.06.0842-00]
- Programa de Pos Graduacao em Ciencias Biologicas at UFOP
- UFOP/PROPP 19/2020 [23109.000929/2020-88]
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This study aimed to investigate the long-term behavioral and neurochemical effects of GUO in a mouse model of depression induced by bilateral bulbectomy (OBX), showing beneficial neurochemical outcomes relevant to counteract depression.
Major depressive disorder (MDD) leads to pervasive changes in the health of afflicted patients. Despite advances in the understanding of MDD and its treatment, profound innovation is needed to develop fast-onset antidepressants with higher effectiveness. When acutely administered, the endogenous nucleoside guanosine (GUO) shows fast-onset antidepressant-like effects in several mouse models, including the olfactory bulbectomy (OBX) rodent model. OBX is advocated to possess translational value and be suitable to assess the time course of depressive-like behavior in rodents. This study aimed at investigating the long-term behavioral and neurochemical effects of GUO in a mouse model of depression induced by bilateral bulbectomy (OBX). Mice were submitted to OBX and, after 14 days of recovery, received daily (ip) administration of 7.5 mg/kg GUO or 40 mg/kg imipramine (IMI) for 45 days. GUO and IMI reversed the OBX-induced hyperlocomotion and recognition memory impairment, hippocampal BDNF increase, and redox imbalance (ROS, NO, and GSH levels). GUO also mitigated the OBX-induced hippocampal neuroinflammation (IL-1, IL-6, TNF-alpha, INF-gamma, and IL-10). Brain microPET imaging ([F-18]FDG) shows that GUO also prevented the OBX-induced increase in hippocampal FDG metabolism. These results provide additional evidence for GUO antidepressant-like effects, associated with beneficial neurochemical outcomes relevant to counteract depression.
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