Exposure to Environmental Complexity Promotes Recovery of Cognitive Function after Traumatic Brain Injury

Abstract

This study was designed to determine whether exposure to a complex environment after traumatic brain injury (TBI) would promote the recovery of cognitive function. Rats were injured at a moderate level of fluid percussion injury (2.1 atm) or were prepared for injury but were not injured (sham injury). Immediately after the injury or sham injury, the injured/complex (n = 8) and the sham/complex (n = 7) groups were placed into a complex environment. The complex environment was a 89 x 89-cm enclosure with different types of bedding and objects that provided motor, olfactory, tactile, and visual stimulation. The injured/standard (n = 8) and the sham/standard (n = 8) groups were returned to the animal vivarium where they were housed individually in standard wire mesh cages (24 x 20 x 18 cm). On days 11-15 (postinjury), performance in the Morris water maze was assessed. Analysis of the latency to reach the goal platform indicated that injured animals recuperating in the complex environment performed significantly better than injured animals recovering in the standard environment (p < 0.01). In fact, injured animals in the complex environment performed as well as both sham-injured groups. The improved performance of injured rats recovering in the enriched environment occurred in the absence of environmentally induced alterations in brain weight. These results indicate that exposure to environmental complexity enhances recovery of cognitive function after TBI.

Environmental enrichment increases progenitor cell survival in the dentate gyrus following lateral fluid percussion injury

“…There was also a significant main effect of group [F(2,27) = 18.93, p < 0.001), but not a group by trial interaction. Post hoc tests indicated that the FP+EE group and the sham group performed significantly better than the FP group (p < 0.001), which is in agreement with previous studies [28,35,59]. Swim speeds did not vary between groups.…”

“…To determine if the experimental manipulations that we used in this study for the EE (1 h/d X 3 weeks) produced improvements in behavior following FP injury similar to those reported in previous studies (24 h/d X 2 weeks) [28,35,59], we added additional animals to the study and evaluated spatial learning and memory in a MWM across groups. In general, performance improved over trial blocks [F(3,36) = 32.75, p <0.001] for all groups (Fig.…”

“…Environmental enrichment (EE) is a well established intervention for attenuating cognitive deficits associated with FP injury [4,28,35,59,76], as well as other experimental brain injury models [13,79]. Although our understanding of how EE mediates functional recovery after brain injury is incomplete, one explanation is that it promotes adaptations of surviving neural networks, enabling them to take over functions of damaged regions of the brain.…”

Evaluation of a Combined Treatment Paradigm Consisting of Environmental Enrichment and the 5-HT1A Receptor Agonist Buspirone after Experimental Traumatic Brain Injury

“…The workshop leaders focused exclusively on the potential for combinatorial pharmacological agents to promote recovery. While this is a commendable start, there is certainly real potential and value in including non-invasive therapies, such as environmental enrichment (EE) or exercise (Gomez-Pinilla et al, 2011;Griesbach et al, 2009;Hamm et al, 1996;Hicks et al, 2002;Hoffman et al, 2008;Kline et al, 2007Kline et al, ,2010Matter et al, 2011;Passineau et al, 2001;de Witt et al, 2011), in combinational therapy paradigms for promoting recovery and perhaps augmenting the pharmacological effects, particularly in rehabilitation settings.…”

“…This paradigm has consistently shown improvements in behavioral and histological outcome after brain trauma and can therefore be considered a reasonable approach to preclinical rehabilitation. Importantly, the benefits conferred by EE span clinically-relevant models of experimental TBI, such as controlled cortical impact (CCI; Chen et al, 2005;de Witt et al, 2011;Hoffman et al, 2008;Kline et al, 2007Kline et al, ,2010Matter et al, 2011;Sozda et al, 2010) and fluid percussion (Hamm et al, 1996;Hicks et al, 2002;Gaulke et al, 2005;Giza et al, 2005;Maegele et al, 2005;Passineau et al, 2001). The second therapy in this combined treatment approach is the systemic administration of the serotonin 1A (5-HT 1A )-receptor agonist buspirone.…”