The role of neurotransmitters and neurohormones in obsessive-compulsive disorder

Abstract

There is considerable evidence that serotonergic systems modulate obsessive-compulsive disorder (OCD) symptomatology. The strongest such data are the antiobsessional effects of serotonin reuptake inhibitors (SRIs), unique among antidepressants. Although the mechanisms underlying the effectiveness of SRI treatment remain largely unknown, the available data support the position that enhanced 5-HT synaptic availability, resulting from a combination of effects on serotonin release and transport, is necessary for the therapeutic efficacy of SRI treatment. The ability of the serotonergic probe mCPP to exacerbate OCD symptoms in untreated patients, and findings that potent 5-HT receptor antagonists may reverse SRI-induced therapeutic benefits, also support serotonergic modulation of OCD symptomatology. There is as yet little evidence that dysregulation in serotonergic systems might be etiologically important in OCD. Although evidence that other neurotransmitter or neuropeptide systems are involved in OCD is considerably more preliminary than that implicating serotonergic mechanisms, there are some indications that such systems may be involved. Studies of the role of these systems, and how they may interact with serotonergic mechanisms, may be particularly helpful in further elucidating the neuropharmacology of OCD and in identifying potential new treatments.