Environmental enrichment cognitive neuroprotection in an experimental model of cerebral ischemia: biochemical and molecular aspects
| Autor: | Rita Gomes Wanderley Pires, Tamara Andrea Alarcon Ferreira, Cristina Martins-Silva, Alice Laschuk Herlinger, Lara Vezula Gonçalves, Juliana Barbosa Coitinho |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Interleukin-1beta Ischemia Hippocampus Environment Neuroprotection Brain Ischemia Brain ischemia 03 medical and health sciences Behavioral Neuroscience Glutamatergic Mice 0302 clinical medicine Cognition Internal medicine medicine Animals Maze Learning Brain-derived neurotrophic factor Environmental enrichment business.industry Brain-Derived Neurotrophic Factor Glutamate receptor Cerebral Infarction medicine.disease Mice Inbred C57BL Stroke Disease Models Animal 030104 developmental biology Endocrinology Memory Short-Term Neuroprotective Agents business 030217 neurology & neurosurgery |
| Zdroj: | Behavioural brain research. 348 |
| ISSN: | 1872-7549 |
| Popis: | Stroke is considered a major cause of global morbidity. Currently, there are no effective treatments for post-stroke cognitive impairment. Enriched environment (EE) has been brought forward as a preconditioning method to induce cerebral tolerance in an ischemic event. However, the subjacent mechanisms involved in this tolerance are not yet clear. Herein we aimed to identify the mechanisms of neuroprotection triggered by EE preconditioning in a murine model of ischemic stroke. In order to do so, C57Bl/6 mice were kept for five weeks either in EE or in standard environment (SC) prior to ischemic injury through bilateral carotid occlusion (BCCAo) or sham surgery. To evaluate cognitive deficits resulting from ischemia, animals were subjected to a set of behavioral test to assess short-term (STM), long-term (LTM) and working memory (WM) performance. Despite no effect of EE having been observed in LTM and WM, EE preconditioning was able to prevent short-term deficits in response to ischemia. This improvement was accompanied by a reduction in the infarct volume in animals following EE pre-exposure. Next, we aimed to analyze the expression of genes involved in cholinergic (M1 and alpha 7 receptors) and glutamatergic (NMDA subunits GluN1, GluN2A, GluN2B and GluN2C) neurotransmission, inflammatory mediators (GFAP and IL-1β) and of the neurotrophin BDNF. Animals tested for STM did not present alterations in the expression of glutamatergic or cholinergic receptors; however, EE was shown to prevent increased expression of IL1-β. On the other hand, in animals submitted to LTM task, EE exposure lead to increased GFAP expression in EE animals that underwent ischemic injury, affecting also the expression of NMDA subunits. In spite of that, no alterations in glutamate content were observed in either group. Altogether, this study suggests that the changes observed in the expression of glutamatergic receptors, the reduction of the inflammatory cytokine IL1-β expression and the increased expression of GFAP in ischemic animals might contribute to the cognitive improvement induced by the EE paradigm. |
| Databáze: | OpenAIRE |
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