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Generation, Purification, and Characterization of Cell-invasive DISC1 Protein Species

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Enhanced dopamine function in DISC1-L100P mutant mice: implications for schizophrenia.

T V Lipina¹, M Niwa, H Jaaro-Peled

¹Samuel Lunenfeld Research Institute at Mount Sinai Hospital, Toronto, Ontario, Canada. lipina@lunenfeld.ca

Genes, Brain, and Behavior

|July 13, 2010

Summary

Disrupted-in-schizophrenia-1 (DISC1) mutation facilitates amphetamine effects in mice, suggesting DISC1

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Area of Science:

Neuroscience
Psychiatric Genetics
Molecular Psychiatry

Background:

Disrupted-in-schizophrenia-1 (DISC1) is implicated in brain function.
Accumulating evidence suggests DISC1 regulates dopamine (DA) pathways.
A specific DISC1 mutation (L100P) induces schizophrenia-related behaviors in mice.

Purpose of the Study:

Investigate the role of dopamine in schizophrenia-related endophenotypes in the DISC1-L100P mouse model.
Elucidate the link between DISC1, dopamine, and schizophrenia pathophysiology.

Main Methods:

Utilized the DISC1-L100P genetic mouse model.
Assessed psychostimulant effects of amphetamine using open field and prepulse inhibition (PPI) tests.
Conducted biochemical studies on striatal dopamine D2 receptors and DA release.
Administered the D2 receptor antagonist haloperidol to evaluate its effects.

Main Results:

Mutant DISC1 (DISC1-L100P) mice exhibited facilitated psychostimulant responses to amphetamine.
Increased striatal D2 receptor proportion (2.1-fold) was observed in mutants without altered in vivo DA release.
Haloperidol treatment reversed hyperactivity, PPI deficits, and latent inhibition (LI) issues, and blocked amphetamine's stimulant effects.

Conclusions:

DISC1 plays a role in D2 receptor-mediated schizophrenia pathophysiology.
Findings support the dopamine hypothesis of schizophrenia by linking DISC1 to DAergic mechanisms.
The DISC1-L100P model provides insights into schizophrenia pathogenesis involving DISC1 and dopamine signaling.