An Enriching Environment : Positive Effects on Autism ?

The effects of enriched environment on BDNF expression in the mouse cerebellum depending on the length of exposure.

Área de Psicobiología, Universidad Jaume I, Castellon de la Plana, España.


Environmental enrichment (EE) has been proposed as a factor that improves neuronal connectivity and brain plasticity.

The induction of molecular mechanisms that takes place in the cortex, nucleus accumbens and hippocampus resulting from exposure to EE has been attributed partly to the role of neurotrophins as brain-derived neurotrophic factor (BDNF). Recent data directly implicate this neurotrophin in the modulation of plasticity changes in the cerebellum produced by living under environmental enrichment.

In the present study, we aimed to assess the effects of different lengths of exposure to EE on cerebellar BDNF expression and western blotting analysis.

On the whole, the present data has shown that BDNF increased under EE.

However, changes in expression as a result of extending the duration of EE were only seen in Purkinje neurons. In Purkinje neurons, long-term exposure was required in order to fully express this neurotrophin.

These data support BDNF as one of the long-term plasticity mechanisms induced by environment, suggesting that cerebellar plasticity can be stimulated as a response to challenges generated by environment.

Our findings could have functional implications for various neurodegenerative disorders such as spinocerebellar ataxias, autism, schizophrenia and certain prion encephalopathies, most of them pathologies which have demonstrated to be characterized by alterations in Purkinje neurons and to show a partial recovery by exposure to EE.


Further Readings of Interest

Enriched rearing improves behavioral responses of an animal model for CNV-based autistic-like traits.

We now report extensive phenotyping with behavioral assays established to evaluate core and associated autistic-like traits, including tests for social abnormalities, ultrasonic vocalizations, perseverative and stereotypic behaviors, anxiety, learning and memory deficits and motor defects. Alterations were identified in both core and associated ASD-like traits. Rearing this animal model in an enriched environment mitigated some, and even rescued selected, neurobehavioral abnormalities, suggesting a role for gene-environment interactions in the determination of copy number variation-mediated autism severity.

Behavioral profiles of mouse models for autism spectrum disorders.

Here, we review the existing data on the phenotypes of mice carrying mutations in genes associated with ASD including neuroligin, neurexin and Shank mutant mice as well as the Fmr1, Mecp2, Ube3a, Nf1, Pten and Tsc1/Tsc2 mutant mice. The diversity and complexity of the phenotype of these mouse models reflect the broad range of phenotypes observed in patients with ASD. Remarkably, results from therapeutic approaches (e.g., modulation of gene expression, administration of pharmacological and nonpharmacological substances, enriched environment) are encouraging since some behavioral alterations could be reversed even when treatment was performed on adult mice. These ongoing studies should therefore increase our understanding of the biological alterations associated with ASD as well as the development of knowledge-based treatments.

Environmental enrichment alters locomotor behaviour and ventricular volume in Mecp2 1lox mice.


Rett syndrome (RTT) is an autistic spectrum developmental disorder associated with mutations in the X-linked Mecp2 gene, and severe behavioural and neuropathological deficits. In a mouse model of RTT (Mecp2(1lox)), we examined whether environmental enrichment (EE) alters behavioural performance and regional brain volume.

At weaning, Mecp2(1lox) and control mice were assigned to enriched or standard housing. From postnatal day 29 to 43, mice were subjected to behavioural tasks measuring motor and cognitive performance. At postnatal day 44, volumes of whole brain, cerebellum, ventricles, and motor cortex were measured using magnetic resonance imaging.

EE provided subtle improvements to locomotor activity and contextual fear conditioning in Mecp2(1lox) mice.

Additionally, EE reduced ventricular volumes, which correlated with improved locomotor activity, suggesting that neuroanatomical changes contribute to improved behaviour.

Our results suggest that post-weaning EE may provide a non-invasive palliative treatment for RTT.

This entry was posted in Autism, Environment, Epigenetics, Genetics, Mice, Neurology, Physiology, Treatment and tagged , , , , , , . Bookmark the permalink.

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