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Updated: Jul 20, 2026

Signal Attenuation as a Rat Model of Obsessive Compulsive Disorder
Published on: January 9, 2015
Is obsessive-compulsive disorder caused by a second-messenger imbalance?
D Marazziti1, J Perez, G B Cassano
1Department of Psychiatry, Neurobiology, Pharmacology and Biotechnology, University of Pisa, Pisa, Italy.
Obsessive-compulsive disorder (OCD) may stem from an imbalance between protein kinase C (PKC) and protein kinase A (PKA) pathways. This imbalance, favoring PKC, suggests new therapeutic targets for OCD treatment.
Area of Science:
- Neuroscience
- Psychiatry
- Molecular Biology
Background:
- Obsessive-compulsive disorder (OCD) is a common psychiatric condition with an unknown etiology.
- Existing research suggests the involvement of the serotonin (5-HT) transporter in OCD.
- Studies indicate reduced platelet 5-HT transporter functionality in OCD patients.
Purpose of the Study:
- To investigate the roles of protein kinase C (PKC) and protein kinase A (PKA) in OCD.
- To propose a unifying hypothesis for the underlying molecular mechanisms of OCD.
Main Methods:
- Combined data from two independent studies of OCD patients.
- Assessed the activity levels of PKC and PKA in patient samples.
Main Results:
- Observed increased activity of protein kinase C (PKC) in OCD patients.
- Observed decreased activity of protein kinase A (PKA) in OCD patients.
Conclusions:
- Hypothesize that OCD may result from an imbalance between PKC and PKA signaling pathways.
- Suggests a prevalence of the phosphoinositide pathway over the cyclic adenosine monophosphate (cAMP) pathway in OCD.
- This hypothesis opens avenues for novel therapeutic interventions for OCD.
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