Environmental Enrichment Protects against Functional Deficits caused by Traumatic Brain Injury

Abstract

Environmental enrichment (EE) increases cortical weight, neuronal density, dendritic branching, and angiogenesis, all of which may be critical for functional recovery following insult. Our study was designed to determine possible benefits of pre-exposure to EE in preventing functional deficits following traumatic brain injury (TBI) to the prefrontal cortex. To examine the benefit of EE, adult male rats were placed in an enriched environment for 15 days. Enrichment was provided through social interaction, exercise, olfactory stimulation, and new objects/toys to explore. Following enrichment, experimental and age-matched controls were subjected to a moderate medial prefrontal cortex injury via controlled cortical impact (CCI). After 1 week recovery, animals were behaviorally tested to assess memory, anxiety, and sensory neglect. Lesion-induced deficits in spatial memory [Morris water maze (MWM)] were significantly attenuated in EE pre-exposed rats 18-21 days following injury. In addition, TBI-induced sensory neglect was significantly reduced in EE rats relative to non-enriched animals. No differences in anxiety-like behavior on the elevated plus maze (EPM) were detected. The behavioral data suggest that EE is neuroprotective when applied prior to TBI, resulting in improved recovery following injury.

RETRACTED ARTICLE: Decreased neuroinflammation and increased brain energy homeostasis following environmental enrichment after mild traumatic brain injury is associated with improvement in cognitive function

“…In general EE refers to conditions that provide increased social, cognitive, and physical stimulation [ 16 , 17 ]. Reports show that EE can exert positive effects on behavioral recovery after cerebral ischemia [ 18 - 21 ], mild TBI [ 22 - 25 ], and neurodegenerative disorders [ 26 , 27 ]. Even though the effects of EE in modulating neuroinflammation is just beginning to be explored [ 28 ], the impact of EE in modulating brain energy homeostasis after mTBI has not been studied.…”

Tracing the trajectory of behavioral impairments and oxidative stress in an animal model of neonatal inflammation

“…Previously, EE has mitigated various animal models of disease and trauma (Dahlqvist et al, 2004;Spires et al, 2004;Johnson et al, 2013;Connors et al, 2014), and increased social behavior (Morley-Fletcher et al, 2003;Schneider et al, 2006) and preference directed toward animals reared in this condition (Mitra and Sapolsky, 2012). Although EE seemed to prevent further nLPS-induced reductions in social behavior, overall sociability levels were lower in EE animals than we anticipated.…”

Environmental enrichment mitigates the sex-specific effects of gestational inflammation on social engagement and the hypothalamic pituitary adrenal axis-feedback system

“…This housing environment has also been attributed to the prevention and reversal of the detrimental effects of a variety of challenges to the adult nervous system. For example, EE has been reported to delay motor deficits in an animal model of Huntington's Disease (Spires et al, 2004), rescue sensorimotor and spatial memory impairments after stroke (Dahlqvist et al, 2004;Ohlsson and Johansson, 1995), attenuate inflammation and the associated physiological and cognitive disruptions that accompany infection (Jurgens and Johnson, 2012;Kentner et al, 2008), and prevent functional deficits following traumatic brain injury (Johnson et al, 2013). There is also a report that EE counteracts the decreased social exploration and latency that accompanies prenatal valproic acid exposure (Schneider et al, 2006), which attenuates proinflammatory cytokines and reactive oxygen species (Cardinale et al, 2010).…”