Long-term effects of environmental stimulation following hypoxia–ischemia on the oxidative state and BDNF levels in rat hippocampus and frontal cortex

Pereira, Lenir Orlandi; Nabinger, Patrícia Machado; Strapasson, Atahualpa Cauê Paim; Nardin, Patrícia; Gonçalves, Carlos Alberto; Siqueira, Ionara Rodrigues; Netto, Carlos Alexandre

doi:10.1016/j.brainres.2008.10.017

Cited by 56 publications

(43 citation statements)

References 54 publications

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“…Based on these findings, it is possible that the neuroprotective effects of EE may be caused by the attenuation of oxidative damage, given the role of oxidative stress in neurodegeneration. Nevertheless, our findings are in contrast with a recent report that did not show any EE effects in modulating levels of thiobarbituric acid reactive substances (marker for oxidative damage) and superoxide dismutase (antioxidant enzyme) in adult rats subjected to hypoxiaischemia as neonates (Pereira et al, 2009). The difference in findings between our current project and the reports on the hypoxia-ischemia model may be explained by the timing of EE housing and evaluation of oxidative damage.…”

Section: Figcontrasting

confidence: 57%

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Briones

Rogozinska

Woods

2011

Journal of Neurotrauma

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In this study, we examined whether enriched environment (EE) housing has direct neuroprotective effects on oxidative damage following transient global cerebral ischemia. Fifty-two adult male Wistar rats were included in the study and received either ischemia or sham surgery. Once fully awake, rats in each group were randomly assigned to either: EE housing or socially paired housing (CON). Animals remained in their assigned environment for 7 days, and then were killed. Our data showed that glutamate receptor expression was significantly higher in the hippocampus of the ischemia CON group than in the ischemia EE group. Furthermore, the oxidative DNA damage, protein oxidation, and neurodegeneration in the hippocampus of the ischemia CON group were significantly increased compared to the ischemia EE group. These results suggest that EE housing possibly modulated the ischemia-induced glutamate excitotoxicity, which then attenuated the oxidative damage and neurodegeneration in the ischemia EE rats.

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Section: Figcontrasting

confidence: 57%

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Briones

Rogozinska

Woods

2011

Journal of Neurotrauma

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“…1a, b). Pereira et al (2009) previously in his report demonstrated that EE has no significant effect on oxidative status of brain following HI. In our study too, we observed no significant effect of EE on oxidative stress parameters during exposure to HH.…”

Section: Discussionmentioning

confidence: 90%

Enriched Environment Prevents Hypobaric Hypoxia Induced Neurodegeneration and is Independent of Antioxidant Signaling

et al. 2012

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Hypobaric hypoxia (HH) induced neurodegeneration has been attributed to several factors including increased oxidative stress, glutamate excitotoxicity, decreased growth factors, apoptosis, etc. Though enriched environment (EE) has been known to have beneficial effects in various neurological disorders, its effect on HH mediated neurodegeneration remains to be studied. Therefore, the present study was conducted to explore the effect of EE on HH induced neurodegeneration. Male Sprague-Dawley rats were placed in enriched and standard conditions during exposure to HH (7 days) equivalent to an altitude of 25,000 ft. The effect of EE on oxidative stress markers, apoptosis, and corticosterone level in hippocampus was investigated. EE during exposure to HH was found to decrease neurodegeneration as evident from decreased caspase 3 expression and LDH leakage. However, no significant changes were observed in ROS, MDA, and antioxidant status of hippocampus. HH elevates corticosterone level and affected the diurnal corticoid rhythm which may contribute to neurodegeneration, whereas EE ameliorate this effect. Because of the association of neurotrophins and stress and/or corticosterone the BDNF and NGF levels were also examined and it was found that HH decreases their level but concurrent exposure to EE maintains their level. Moreover, inhibition of Tyrosine kinase receptor (Trk) with K252a nullifies the protective effect of EE, whereas Trk activation with agonist, amitriptyline showed protective effect similar to EE. Taken together, we conclude that EE has a potential to ameliorate HH mediated neuronal degeneration which may act through antioxidant independent pathway by modulation of neurotrophins.

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“…In contrast, males, but not females, exhibited EE-enhanced spatial memory performance. 89 Given that EE produces many changes in the brain, it seemed unlikely that the EE benefits were confined only to males, particularly because several studies in other CNS injury models, [90][91][92] as well as non-CNS injury paradigms, [93][94][95] have consistently reported that EE induces cognitive benefits in females. Hence, to further address this disparity, Monaco and colleagues 96 set out to reassess the effect of EE on functional and histological outcome in female rats after brain trauma, using similar experimental procedures to the previous study by Wagner and colleagues.…”

Section: The Benefits Of Environmental Enrichment Extend Beyond Adultmentioning

confidence: 99%

Environmental Enrichment as a Viable Neurorehabilitation Strategy for Experimental Traumatic Brain Injury

Bondi

Klitsch

Leary

et al. 2014

Journal of Neurotrauma

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Environmental enrichment (EE) emerged as a robust independent variable capable of influencing behavioral outcome in experimental studies after the fortuitous observation by renowned neuropsychologist Donald O. Hebb that rats raised as pets in his home performed markedly better on problem-solving tasks than those kept in the laboratory. In the subsequent years, numerous studies ensued demonstrating that EE was also capable of inducing neuroplasticity in normal (i.e., noninjured) rats. These behavioral and neural alterations provided the impetus for investigating EE as a potential therapy for traumatic brain injury (TBI), which, over the past two decades, has resulted in several reports. Hence, the aim of this review is to integrate the findings and present the current state of EE as a viable neurorehabilitation strategy for TBI. Using the specific key term searches ''traumatic brain injury'' and ''environmental enrichment'' or ''enriched environment,'' 30 and 30 experimental TBI articles were identified by PubMed and Scopus, respectively. Of these, 27 articles were common to both search engines. An additional article was found on PubMed using the key terms ''enriched environment'' and ''fluid percussion.'' A review of the bibliographies in the 34 articles did not yield additional citations. The overwhelming consensus of the 34 publications is that EE benefits behavioral and histological outcome after brain injury produced by various models. Further, the enhancements are observed in male and female as well as adult and pediatric rats and mice. Taken together, these cumulative findings provide strong support for EE as a generalized and robust preclinical model of neurorehabilitation. However, to further enhance the model and to more accurately mimic the clinic, future studies should continue to evaluate EE during more rehabilitation-relevant conditions, such as delayed and shorter time periods, as well as in combination with other therapeutic approaches, as we have been doing for the past few years.

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Long-term effects of environmental stimulation following hypoxia–ischemia on the oxidative state and BDNF levels in rat hippocampus and frontal cortex

Cited by 56 publications

References 54 publications

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Modulation of Ischemia-Induced NMDAR1 Activation by Environmental Enrichment Decreases Oxidative Damage

Enriched Environment Prevents Hypobaric Hypoxia Induced Neurodegeneration and is Independent of Antioxidant Signaling

Environmental Enrichment as a Viable Neurorehabilitation Strategy for Experimental Traumatic Brain Injury

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