Serotonin, obsessive compulsive disorder and the basal ganglia

Summary

Evidence suggests that there is dysfunction in limbic cortico-striato-pallido-thalamic circuitry in obsessive compulsive disorder (OCD). Serotonin receptors are certainly positioned to modulate activity within this ‘limbic loop’, either via 5-HT_2A-mediated reductions in striatal dopamine release, 5-HT_1D-mediated reductions in pallidal or nigral GABA release from striatal projection neurons, or via 5-HT₃- or 5-HT_1A-mediated reductions in cellular activity within limbic cortico-striatal projection neurons. Other models of neuroanatomic substrates utilizing other neurotransmitter systems are also discussed to explain the possible basis of neuronal dysfunction in OCD.