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Reelin down-regulation in mice and psychosis endophenotypes
Patricia Tueting1, Mohemed-Salim Doueiri, Alessandro Guidotti
1Psychiatric Institute, University of Illinois at Chicago, 1601 West Taylor Street Chicago, IL 60612, USA. ptueting@psych.uic.edu
Neuroscience and Biobehavioral Reviews
|June 14, 2006
Summary
Reelin protein deficiency in mice models psychosis. Epigenetic changes, like DNA hypermethylation, mimic these brain and behavioral abnormalities, offering insights into psychosis development.
Area of Science:
- Neuroscience
- Psychiatry
- Genetics
Background:
- Reelin, a glycoprotein crucial for neuronal development and plasticity, is downregulated in psychosis.
- The reeler heterozygous mouse (+/rl) exhibits brain abnormalities mirroring those in psychotic brains.
- These abnormalities include reduced GAD67, altered dendritic structures, and impaired synaptic function.
Purpose of the Study:
- To investigate the role of Reelin downregulation in psychosis.
- To explore the potential of the reeler heterozygous mouse as a model for psychosis.
- To examine the interplay between genetic and epigenetic factors in psychosis.
Main Methods:
- Comparative analysis of brain abnormalities in reeler heterozygous mice and postmortem psychotic brains.
- Investigation of DNA methylation patterns in Reelin (RELN) and GAD67 promoters.
- Induction of hypermethylation using methionine treatment in mice.
Main Results:
- Reelin deficiency in +/rl mice leads to brain changes similar to psychosis.
- Hypermethylation of RELN and GAD67 promoters is observed in psychotic brains and can be induced experimentally.
- Methionine-induced hypermethylation replicates brain and behavioral phenotypes of +/rl mice.
Conclusions:
- The reeler heterozygous mouse is a valuable model for studying psychosis.
- Epigenetic mechanisms, particularly DNA hypermethylation, play a significant role in Reelin downregulation and psychosis.
- Combining genetic and epigenetic factors is crucial for understanding the etiology of psychosis.
