Post-Ischemic Housing Conditions Influence On Gene Transcription And Translation After Permanent Focal Brain Ischemia In Rats

Forskningsoutput: AvhandlingDoktorsavhandling (sammanläggning)


Enriched environment (EE) housing significantly ameliorates neurological deficits induced by cortical brain ischemia without changing infarction size, suggesting that EE-related functional benefits are associated with neuronal plasticity events in the remaining tissue. Brain-derived neurotrophic factor (BDNF), nerve growth factor-induced gene A (NGFI-A) and corticosteroid receptors (mineralocorticoid receptor, MR; glucocorticoid receptor, GR) have been demonstrated to be involved in brain plasticity. The purpose of this thesis was to determine if post-ischemic housing conditions had a significant effect on transcription and/or translation of BDNF, NGFI-A and corticosteroid receptors. We found that BDNF gene was down regulated in EE-housed rats when compared to the rats housed in standard cages at 2~12 days after cortical brain ischemia in peri-infarct cortex, contralateral cortex and bilateral hippocampus. The protein level of BDNF in the ipsilateral frontal cortex was lower in the EE-housed rats than the standard environment (SE)-housed rats at 12d postischemia. The mRNA expression of NGFI-A showed a similar pattern of BDNF except for an increase at 30 d after induction of brain ischemia in EE-housed rats. Ischemia-induced reduction of GR was prevented in the rats housed in EE condition. There was no difference between EE- and SE-housed animals in MR gene expression. Gene expressions, however, are very complex in housing conditions and postischemia. Whether EE-related gene transcription and/or translation reported in this thesis are linked with EE-induced functional benefits to brain ischemia, further studies need be conducted.


  • Li-Ru Zhao
Enheter & grupper

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Neurologi


Tilldelande institution
Handledare/Biträdande handledare
  • [unknown], [unknown], handledare, Extern person
Tilldelningsdatum2004 sep 15
  • Department of Clinical Neuroscience, Lund University
Tryckta ISBN91-628-6171-9
StatusPublished - 2004


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