Brain Weight Increases Resulting from Environmental Enrichment: A Directional Dominance in Mice
A genetic analysis of brain weights of 544 mice reared in either enriched or standard laboratory environments indicated significant directional dominance in the percentage of increase in brain weight as a result of enrichment.
[Show abstract] [Hide abstract] 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.0Comments 27Citations
- "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). Early studies in rodents indicate that EE increases total brain and cortical weight (Henderson, 1970; Rosenzweig and Bennett, 1972; Rosenzweig et al., 1972). Subsequent studies document additional benefits of EE including increased neuronal density (Kempermann et al., 1997), dendritic branching (Greenough and Volkmar, 1973), cortical tissue synapses (Turner and Greenough, 1985), neuronal transmission (Rampon et al., 2000), and enhanced neurotrophic growth factor expression (Young et al., 1999; Ickes et al., 2000). "
[Show abstract] [Hide abstract] ABSTRACT: Information processing, memory formation, or functional recovery after nervous system damage depend on the ability of neurons to modify their functional properties or their connections. At the cellular/molecular level, structural modifications of neural circuits are finely regulated by intrinsic neuronal properties and growth-regulatory cues in the extracellular milieu. Recently, it has become clear that stimuli coming from the external world, which comprise sensory inflow, motor activity, cognitive elaboration, or social interaction, not only provide the involved neurons with instructive information needed to shape connection patterns to sustain adaptive function, but also exert a powerful influence on intrinsic and extrinsic growth-related mechanisms, so to create permissive conditions for neuritic remodeling. Here, we present an overview of recent findings concerning the effects of experience on molecular mechanisms underlying CNS structural plasticity, both in physiological conditions and after damage, with particular focus on activity-dependent modulation of growth-regulatory genes and epigenetic modifications.0Comments 12Citations
- "" It refers to housing conditions that facilitate sensory, motor, cognitive, and social stimulation (i.e., a large cage containing various objects, tubes, and running wheels, in which a numerous colony of individuals is housed). In the initial studies, the effects of environmental stimuli on parameters such as total brain weight (Bennett et al., 1969; Henderson, 1970 Henderson, , 1973 Ferchmin and Bennett, 1975), total DNA or RNA content (Mushynski et al., 1973; Uphouse and Bonner, 1975; Henderson, 1976), or total brain proteins were measured (Levitan et al., 1972; Jørgensen and Bock, 1979). Subsequently, many studies have shown that environmental stimulation elicits a variety of plastic modifications in the adult brain, ranging from synaptic remodeling and dendritic growth (Greenough et al., 1985; Beaulieu and Colonnier, 1987) to gliogenesis (Altman and Das, 1964; Diamond et al., 1966; Szeligo and Leblond, 1977 ), angiogenesis (Black et al., 1990; Isaacs et al., 1992; Kleim et al., 1996; Swain et al., 2003), and neurogenesis (Kempermann et al., 1997Kempermann et al., , 1998 Gould et al., 1999; Van Praag et al., 1999; Ambrogini et al., 2000). "
[Show abstract] [Hide abstract] ABSTRACT: This experiment was carried out to investigate the long-term effects of enhancing cage complexity on behavioural measures of welfare in laboratory rats. We housed 72 rats in groups of four in either 'enriched' or 'unenriched' cages for six weeks. Scan and focal animal sampling were conducted in both the light and dark phase of the second, fourth and sixth weeks. Results revealed that rats in the 'enriched' cages showed longer durations of sleep behaviour, and low levels of agonistic behaviour compared to rats in the 'unenriched' cages. Results importantly demonstrated that the behavioural changes observed in the enriched environment were due to the presence of the enrichments themselves in the cages (indirect effects) and not due merely to rats interacting with the enrichment items in their environment. Thus, enhancing the complexity of conventional laboratory cages can promote behaviour such as longer bouts of sleep that is likely to be indicative of good welfare, and diminish levels of behaviour such as aggression that is likely to lead to poor welfare.0Comments 22Citations
- "Cage-size is another frequently encountered confounding variable , with enriched groups typically provided with not just more cage furniture, but also more space (e.g. Bennett et al., 1969; Black et al., 1989; Henderson, 1970; Huck and Price, 1975; Kiyono et al., 1981; Mirmiran et al., 1982; Moncek et al., 2004; Patterson-Kane et al., 1999; Van Gool and Mirmiran, 1986; Volkmar and Greenough, 1972). It is therefore hard to determine whether findings are the result of supplying standard laboratory cages with additional items, and/or a consequence of the additional floor space and increased cage height. "
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