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Behavioral changes in G72/G30 transgenic mice.

David M Otte¹, Andras Bilkei-Gorzó, Michaela D Filiou

¹Institute of Molecular Psychiatry, University of Bonn, Sigmund-Freud-Strasse 25, Bonn, Germany.

European Neuropsychopharmacology : the Journal of the European College of Neuropsychopharmacology

|February 5, 2009

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The human G72/G30 gene, linked to psychiatric disorders, was expressed in mice. These G72Tg mice showed behaviors relevant to schizophrenia and other mental health conditions.

Area of Science:

Neuroscience
Genetics
Psychiatry

Background:

The G72/G30 gene locus is primate-specific and implicated in schizophrenia, bipolar, and panic disorders.
The encoded LG72 protein's function is debated, with roles suggested in peroxisomal enzyme regulation or mitochondrial fragmentation.

Purpose of the Study:

To investigate the in vivo function of the human G72/G30 gene locus.
To create and characterize a "humanized" mouse model (G72Tg) expressing G72 and G30 transcripts and the LG72 protein.

Main Methods:

Generation of BAC transgenic mice (G72Tg) expressing human G72/G30.
Assessment of G72 expression patterns in the G72Tg mouse brain.
Behavioral testing of G72Tg mice for sensorimotor gating, PCP sensitivity, motor coordination, compulsive behaviors, and olfactory identification.

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Main Results:

G72 expression was prominent in the cerebellum, hippocampus, cortex, and olfactory bulb of G72Tg mice.
G72Tg mice exhibited deficits in sensorimotor gating, increased PCP sensitivity, motor coordination issues, compulsive behaviors, and impaired smell identification.
Sensorimotor gating deficits were reversed by haloperidol treatment.

Conclusions:

The human G72/G30 gene locus, when expressed in mice, induces behavioral phenotypes relevant to psychiatric disorders.
G72Tg mice serve as a valuable model for studying the neurobiological underpinnings of these conditions and for testing potential therapeutic interventions.