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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/25535

Title: Deficiency in MBD2 is Sufficient to Cause Behavioral Impairments in Mice
Authors: Zavalishina, Lidiya
Advisor: Eubanks, James
Department: Physiology
Keywords: MBD2
behavioral impairments
MeCP2
EEG
Issue Date: 31-Dec-2010
Abstract: Methyl-CpG-binding proteins (MeCP2, MBD1-MBD3) recruit transcriptional co-repressor molecules to methylated regions and silence transcription. The role of MBD2 in regulating brain function and behavior remains largely unexamined. To begin elucidating whether MBD2 influences neural function, I assessed the behavioral performance of Mbd2 null mice, compared their hippocampal electroencephalographic activity during exploration, and performed protein and mRNA expression assessments. The results indicate that mutant mice display a heightened anxiety-like behavior, diminished explorative activity and reduced sociability compared to wild-type mice. However, these behavioral differences were not paralleled by neurophysiological impairments. Mutant hippocampal and cortical samples display significantly elevated MeCP2 mRNA levels. Yet, MeCP2 protein expression did not mirror the mRNA profile and instead was significantly reduced. Glucocorticoid Receptor mRNA levels were significantly reduced in the hippocampus and cortex regions of Mbd2 null brains. The loss of MBD2 is sufficient to induce behavioral impairments in mice without introducing gross deficits in hippocampal neurophysiology.
URI: http://hdl.handle.net/1807/25535
Appears in Collections:Master
Department of Physiology - Master theses

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