Long-term changes in metabolic brain network drive memory impairments in rats following neonatal hypoxia-ischemia
| Autor: | Andrey Vinicius Soares, Carlos Alexandre Netto, Gabriele Zanirati, Guilherme Schu, Gianina Teribele Venturin, Pamella Nunes Azevedo, Samuel Greggio, Felipe Kawa Odorcyk, Gabriela de Oliveira Laguna, Eduardo R. Zimmer, Luz Elena Durán–Carabali, Jaderson Costa da Costa |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Male
medicine.medical_specialty Cognitive Neuroscience Ischemia Morris water navigation task Experimental and Cognitive Psychology Brain damage Hippocampal formation 050105 experimental psychology 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine Internal medicine Neuroplasticity medicine Animals 0501 psychology and cognitive sciences Rats Wistar Cognitive deficit Memory Disorders business.industry 05 social sciences Brain Hypoxia (medical) medicine.disease Rats Disease Models Animal Glucose Endocrinology Positron-Emission Tomography Hypoxia-Ischemia Brain Brain size Nerve Net medicine.symptom business Neuroscience 030217 neurology & neurosurgery |
| Zdroj: | Neurobiology of Learning and Memory. 171:107207 |
| ISSN: | 1074-7427 |
| DOI: | 10.1016/j.nlm.2020.107207 |
| Popis: | Background and purpose Hypoxia and cerebral ischemia (HI) events are capable of triggering important changes in brain metabolism, including glucose metabolism abnormalities, which may be related to the severity of the insult. Using positron emission microtomography (microPET) with [18F]fluorodeoxyglucose (18F-FDG), this study proposes to assess abnormalities of brain glucose metabolism in adult rats previously submitted to the neonatal HI model. We hypothesize that cerebral metabolic outcomes will be associated with cognitive deficits and magnitude of brain injury. Methods Seven-day-old rats were subjected to an HI model, induced by permanent occlusion of the right common carotid artery and systemic hypoxia. 18F-FDG-microPET was used to assess regional and whole brain glucose metabolism in rats at 60 postnatal days (PND 60). An interregional cross-correlation matrix was utilized to construct metabolic brain networks (MBN). Rats were also subjected to the Morris Water Maze (MWM) to evaluate spatial memory and their brains were processed for volumetric evaluation. Results Brain glucose metabolism changes were observed in adult rats after neonatal HI insult, limited to the right brain hemisphere. However, not all HI animals exhibited significant cerebral hypometabolism. Hippocampal glucose metabolism was used to stratify HI animals into HI hypometabolic (HI-h) and HI non-hypometabolic (HI non-h) groups. The HI-h group had drastic MBN disturbance, cognitive deficit, and brain tissue loss, concomitantly. Conversely, HI non-h rats had normal brain glucose metabolism and brain tissue preserved, but also presented MBN changes and spatial memory impairment. Furthermore, data showed that brain glucose metabolism correlated with cognitive deficits and brain volume outcomes. Conclusions Our findings demonstrated that long-term changes in MBN drive memory impairments in adult rats subjected to neonatal hypoxic ischemia, using in vivo imaging microPET-FDG. The MBN analyses identified glucose metabolism abnormalities in HI non-h animals, which were not detected by conventional 18F-FDG standardized uptake value (SUVr) measurements. These animals exhibited a metabolic brain signature that may explain the cognitive deficit even with no identifiable brain damage. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect