A CRH-HCN Theory of Obsessive-Compulsive Disorder (OCD)

TL;DR

This paper proposes a comprehensive neurochemical theory of OCD, linking stress-related CRH release, cAMP activation, and HCN channel activity to the core symptoms of obsessions and compulsions.

Contribution

It introduces the first complete neurochemical model of OCD, connecting stress hormones to neural firing patterns underlying OCD behaviors.

Findings

CRH release in the prefrontal cortex triggers OCD symptoms.

Activation of HCN channels promotes compulsive neural firing.

The theory explains diverse OCD features through neurochemical interactions.

Abstract

I present the first complete theory of OCD. OCD occurs when excessive CRH is released in the prefrontal cortex, activating cAMP. cAMP is a major inducer of HCN channels, which promote repeated neural firing. The combination of CRH, which is strongly associated with stress, and repeated firing that cannot be controlled, explains all of the features of OCD, including obsessions and compulsions of all kinds.