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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.
Highlights
Four rats were excluded from all analyses (1 standard control (ST)-traumatic brain injury (TBI), and 3 Sham) due to death or poor post-surgical recovery, resulting in the following sample sizes for behavioral analysis: 16 enriched condition (EC)-TBI, 15 ST-TBI, and 13 Sham
It is important to note that prefrontal damage can increase risk-taking behavior (Bechara et al, 1994; Floden et al, 2008) which may result in increased open arm time via a non-anxiety related mechanism (Pandey et al, 2009)
Post-hoc analysis indicated that both Sham and EC-TBI removed the stickers significantly faster than the ST-TBI group at both post-injury time points (Figure 3)
Summary
Environmental enrichment (EE), the provision of a rich and stimulating environment, induces neuronal changes that can ameliorate functional deficits associated with various degenerative diseases and injury (Horner and Gage, 2000; van Dellen et al, 2000; Passineau et al, 2001; Will et al, 2004; Gaulke et al, 2005). The beneficial effects of EE on cortical structure and function support its use as a therapy to improve recovery from traumatic brain injury (TBI) (Will et al, 1977, 2004; Horner and Gage, 2000; Passineau et al, 2001; Chen et al, 2005; Gaulke et al, 2005; Giza et al, 2005; Wagner et al, 2005; Kline et al, 2007). The cognitive benefits of EE are demonstrated by a reduced deficit in memory performance following brain injury (Hamm et al, 1996; Will et al, 2004; Komitova et al, 2005)
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