Early Environmental Enrichment May Alleviate Neuronal and Behavioral Deficits in MeCP2 Model of ASD
Autism Spectrum disorder (ASD) is a developmental disorder characterized by impairment in learning and memory processes, synaptic plasticity, as well as social communication deficits and pronounced anxiety. Studies have demonstrated that mutations of methyl-CpG binding protein 2 (MeCP2), a neuroepigenetic factor, in mice causes cognitive and behavioral impairments seen in clinical populations of ASD. The purpose of this study was to determine if early intervention may not only improve behavioral deficits bit also promote neuronal health by increasing levels of a neurotrophic factor known as brain-derived neurotrophic factor (BDNF) in our MeCP2 knockout (KO) mice, a transgenic animal model of ASD. KO and wildtype (WT) mice were randomly assigned to either environmental enriched (EE) or single housed (SH) conditions. In EE housing, mice were exposed to different running wheels, textures, toys and grouped housed. In the SH condition, mice were singly housed without access to any environmental enrichment or nestlets. After 12 weeks, elevated plus maze (EPM) and dark-light test (DLT) were used to assess for anxiety-like behavior, as well as social interaction (SI). KO – EE displayed reduced anxiety-like behaviors. Hippocampal brain derived neurotrophic factor (BDNF) levels was also significantly increased in KO-EE mice, relative to KO-SH mice. This suggest improved neuroplasticity important for memory and learning. Additionally, KO-EE mice displayed increased social interactions. Overall, these finding suggest MeCP2 mouse model of ASD had alleviated physiological and behavioral deficits when exposed to early interventions. Texas Woman's University Startup Funds. The Woodcock Institute for the Advancement of Neurocognitive Research and Applied Practice. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Authors
- Elisa S. Na (ORCID: https://orcid.org/0000-0001-7236-9868)
- Priscila Frayre (ORCID: https://orcid.org/0000-0003-1221-0155)
- S. Vásquez (ORCID: https://orcid.org/0000-0002-0183-0335)
Institutions
- Texas Woman's University (US)
Publication Details
- Journal
- Physiology
- Published
- 2025-05-01
- DOI
- https://doi.org/10.1152/physiol.2025.40.s1.1594
- Primary Topic
- Genetics and Neurodevelopmental Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00