title: Environmental complexity and central nervous system development and function.
abstract: Environmental restriction or deprivation early in development can induce social, cognitive, affective, and motor abnormalities similar to those associated with autism. Conversely, rearing animals in larger, more complex environments results in enhanced brain structure and function, including increased brain weight, dendritic branching, neurogenesis, gene expression, and improved learning and memory. Moreover, in animal models of CNS insult (e.g., gene deletion), a more complex environment has attenuated or prevented the sequelae of the insult. Of relevance is the prevention of seizures and attenuation of their neuropathological sequelae as a consequence of exposure to a more complex environment. Relatively little attention, however, has been given to the issue of sensitive periods associated with such effects, the relative importance of social versus inanimate stimulation, or the unique contribution of exercise. Our studies have examined the effects of environmental complexity on the development of the restricted, repetitive behavior commonly observed in individuals with autism. In this model, a more complex environment substantially attenuates the development of the spontaneous and persistent stereotypies observed in deer mice reared in standard laboratory cages. Our findings support a sensitive period for such effects and suggest that early enrichment may have persistent neuroprotective effects after the animal is returned to a standard cage environment. Attenuation or prevention of repetitive behavior by environmental complexity was associated with increased neuronal metabolic activity, increased dendritic spine density, and elevated neurotrophin (BDNF) levels in brain regions that are part of cortical-basal ganglia circuitry. These effects were not observed in limbic areas such as the hippocampus.
authors.affiliation: McKnight Brain Institute and Department of Psychiatry, University of Florida, Gainesville, Florida 32601, USA. mlewis@psychiatry.ufl.edu
authors.forename: Mark H
authors.initials: MH
authors.lastname: Lewis
mesh_terms: D000818:Animals; D001321:Autistic Disorder; D001921:Brain / Q000098:blood supply; D020520:Brain Infarction / Q000503:physiopathology; D002452:Cell Count; D002493:Central Nervous System Diseases / Q000150:complications / Q000503:physiopathology*; D002648:Child; D003712:Dendrites / Q000648:ultrastructure; D002658:Developmental Disabilities / Q000150:complications / Q000503:physiopathology*; D004777:Environment; D004827:Epilepsy / Q000503:physiopathology; D006801:Humans; D051379:Mice; D009473:Neuronal Plasticity / Q000502:physiology; D013116:Spinal Cord / Q000166:cytology; D013239:Stereotyped Behavior