Limits...
Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury.

Alwis DS, Rajan R - Front Syst Neurosci (2014)

Bottom Line: The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage.These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI).In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Monash University Clayton, VIC, Australia.

ABSTRACT
The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage. Since the initial discovery by Hebb (1947) that environmental enrichment (EE) was able to confer improvements in cognitive behavior, EE has been investigated as a powerful form of experience-dependent plasticity. Animal studies have shown that exposure to EE results in a number of molecular and morphological alterations, which are thought to underpin changes in neuronal function and ultimately, behavior. These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI). In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain. We then extend this review to specifically address the role of EE in the treatment of experimental TBI, where we will discuss the demonstrated sensorimotor and cognitive benefits associated with exposure to EE, and their possible mechanisms. Finally, we will explore the use of EE-based rehabilitation in the treatment of human TBI patients, highlighting the remaining questions regarding the effects of EE.

No MeSH data available.


Related in: MedlinePlus

Behavioral benefits conferred by the timing/duration of EE relative to creation of TBI. The efficacy of EE treatment when administered pre/post-injury is represented by green full-line arrows which indicate EE timing conditions that ameliorated behaviors, while white dashed arrows indicate EE timing conditions that failed to ameliorate behaviors.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4151031&req=5

Figure 2: Behavioral benefits conferred by the timing/duration of EE relative to creation of TBI. The efficacy of EE treatment when administered pre/post-injury is represented by green full-line arrows which indicate EE timing conditions that ameliorated behaviors, while white dashed arrows indicate EE timing conditions that failed to ameliorate behaviors.

Mentions: Some clues as to the potential mechanism by which EE could rescue brain function in TBI comes from the finding that the timing and duration of EE are important factors governing motor and cognitive recovery post-TBI (Figure 2; Hoffman et al., 2008; De Witt et al., 2011; Matter et al., 2011; Cheng et al., 2012). Thus, Hoffman et al. (2008) reported that recovery of motor and cognitive function, such as beam-walking and spatial learning and memory, depended on an optimal time and length of EE exposure relative to time after injury. After mixed focal-diffuse TBI, even a short period of EE exposure (6 h) was sufficient to improve motor and cognitive behavior to a level comparable to the enhanced performance seen after much longer (3 weeks), continuous exposure to EE (Hoffman et al., 2008; De Witt et al., 2011; Matter et al., 2011). The benefits of EE were not dose-dependent, however, as task performance in animals exposed to shorter periods of EE (2 and 4 h) did not differ significantly from those of injured animals housed in standard conditions, suggesting a minimal threshold of EE exposure is needed for beneficial effects (De Witt et al., 2011). EE-induced plasticity has persisting effects such that even limited exposure (3 weeks) to EE post-TBI can result in long-term protection from memory deficits, as assessed by the MWM task, for up to 6 months after animals are withdrawn from EE conditions (Cheng et al., 2012), making it an ideal candidate for therapy post-TBI.


Environmental enrichment and the sensory brain: the role of enrichment in remediating brain injury.

Alwis DS, Rajan R - Front Syst Neurosci (2014)

Behavioral benefits conferred by the timing/duration of EE relative to creation of TBI. The efficacy of EE treatment when administered pre/post-injury is represented by green full-line arrows which indicate EE timing conditions that ameliorated behaviors, while white dashed arrows indicate EE timing conditions that failed to ameliorate behaviors.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4151031&req=5

Figure 2: Behavioral benefits conferred by the timing/duration of EE relative to creation of TBI. The efficacy of EE treatment when administered pre/post-injury is represented by green full-line arrows which indicate EE timing conditions that ameliorated behaviors, while white dashed arrows indicate EE timing conditions that failed to ameliorate behaviors.
Mentions: Some clues as to the potential mechanism by which EE could rescue brain function in TBI comes from the finding that the timing and duration of EE are important factors governing motor and cognitive recovery post-TBI (Figure 2; Hoffman et al., 2008; De Witt et al., 2011; Matter et al., 2011; Cheng et al., 2012). Thus, Hoffman et al. (2008) reported that recovery of motor and cognitive function, such as beam-walking and spatial learning and memory, depended on an optimal time and length of EE exposure relative to time after injury. After mixed focal-diffuse TBI, even a short period of EE exposure (6 h) was sufficient to improve motor and cognitive behavior to a level comparable to the enhanced performance seen after much longer (3 weeks), continuous exposure to EE (Hoffman et al., 2008; De Witt et al., 2011; Matter et al., 2011). The benefits of EE were not dose-dependent, however, as task performance in animals exposed to shorter periods of EE (2 and 4 h) did not differ significantly from those of injured animals housed in standard conditions, suggesting a minimal threshold of EE exposure is needed for beneficial effects (De Witt et al., 2011). EE-induced plasticity has persisting effects such that even limited exposure (3 weeks) to EE post-TBI can result in long-term protection from memory deficits, as assessed by the MWM task, for up to 6 months after animals are withdrawn from EE conditions (Cheng et al., 2012), making it an ideal candidate for therapy post-TBI.

Bottom Line: The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage.These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI).In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Monash University Clayton, VIC, Australia.

ABSTRACT
The brain's life-long capacity for experience-dependent plasticity allows adaptation to new environments or to changes in the environment, and to changes in internal brain states such as occurs in brain damage. Since the initial discovery by Hebb (1947) that environmental enrichment (EE) was able to confer improvements in cognitive behavior, EE has been investigated as a powerful form of experience-dependent plasticity. Animal studies have shown that exposure to EE results in a number of molecular and morphological alterations, which are thought to underpin changes in neuronal function and ultimately, behavior. These consequences of EE make it ideally suited for investigation into its use as a potential therapy after neurological disorders, such as traumatic brain injury (TBI). In this review, we aim to first briefly discuss the effects of EE on behavior and neuronal function, followed by a review of the underlying molecular and structural changes that account for EE-dependent plasticity in the normal (uninjured) adult brain. We then extend this review to specifically address the role of EE in the treatment of experimental TBI, where we will discuss the demonstrated sensorimotor and cognitive benefits associated with exposure to EE, and their possible mechanisms. Finally, we will explore the use of EE-based rehabilitation in the treatment of human TBI patients, highlighting the remaining questions regarding the effects of EE.

No MeSH data available.


Related in: MedlinePlus