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Depressive-like behaviour of mice lacking cellular prion protein
Vinicius M Gadotti1, Stephan P Bonfield, Gerald W Zamponi
1Department of Physiology and Pharmacology, Hotchkiss Brain Institute, University of Calgary, Calgary T2N 4N1, Canada.
Behavioural Brain Research
|March 29, 2011
Summary
Cellular Prion Protein (PrP(C)) deficiency in mice leads to depressive-like behaviors. Antidepressant drugs reversed these behaviors, suggesting PrP(C) is a potential target for depression treatments.
Area of Science:
- Neuroscience
- Psychiatry
- Molecular Biology
Background:
- Cellular Prion Protein (PrP(C)) has known protective roles in neurological conditions like ischemia and epilepsy.
- Limited research exists on the role of PrP(C) in psychiatric disorders, particularly depression.
Purpose of the Study:
- To investigate the potential role of PrP(C) in modulating depressive-like states using a mouse model.
- To explore PrP(C) as a potential therapeutic target for depressive disorders.
Main Methods:
- Utilized PrP(C) null mice and wild-type littermates for behavioral analysis.
- Assessed depressive-like behavior using the Forced Swimming Test (FST) and Tail Suspension Test (TST).
- Administered the antidepressant imipramine and NMDA receptor antagonist MK-801 to evaluate behavioral reversal.
Main Results:
- PrP(C) null mice exhibited significantly increased depressive-like behavior in both FST and TST compared to wild-type controls.
- The antidepressant imipramine and MK-801 effectively reversed the depressive-like behaviors in knockout mice during the TST.
- These findings highlight a critical role for PrP(C) in the modulation of depressive-like states.
Conclusions:
- PrP(C) plays a significant role in regulating mood and depressive-like behaviors in mice.
- The study supports the association of PrP(C) with mood disorder alterations.
- PrP(C) emerges as a promising potential drug target for the development of novel depression therapies.
