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Environmental enrichment induces changes in the mRNA expression of rat EAAC1 and NMDA but not in AMPA

Andin, Josefine (författare)
Linköpings universitet,Geriatrik,Hälsouniversitetet
Hallbeck, Martin (författare)
Mohammed, Abdul (författare)
Division of Geriatric Medicine, Neurontec, Karolinska Institutet, Sweden
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Marcusson, Jan (författare)
Linköpings universitet,Geriatrik,Hälsouniversitetet
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 (creator_code:org_t)
Engelska.
  • Annan publikation (övrigt vetenskapligt/konstnärligt)
Abstract Ämnesord
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  • Interaction with the environment has a key role in refining the neuronal circuitry required for normal brain function throughout life. Profound effects of enriched environment has been shown on neuronal strucrure and chemistry in experimental animals. Epidemiological studies imply that this is true also in man, thus cognitive stimulation has a protective effect on neurodegeneration, e.g. Alzheimer's disease. Glutamatergic corticocortical pathways are imperative for cognitive functions, such as memory and learning, and long term porenriation relies on the AMPA and NMDAglutamate rcceptors. The glutamate signalling is also dependent on a fine-runed transport system, in the hippocampus primarily by theglutamate transporter EAACl. In this study we show how environmental enrichment modulates these parts of the glutamarergic system using in siru hybridization. This work demonstrates for the first time that environmental enrichment modulates the mRNA expression of EAAC1 which is significantly decreased in hippocampal and cortical areas. We also provide further evidence about the upregulation of NMDA mRNA after environmental enrichement, and show it to have a regionally and hemisphere specific regulation. The current work also confirms that AMPA mRNA is nor per se changed by environmental enrichment in adult animals. Taken together, our results extend the knowledge of the glutamatergic system and its modulation by environmental enrichment and could contribute to the development of strategies aimed at limiting pathological changes associated with glutamatergic dysfunctions.

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