SEROTONIN, OBSESSIVE-COMPULSIVE DISORDER AND THE BASAL GANGLIA

Evidence suggests that there is dysfunction in limbic cortico-striato- pallido-thalamic circuitry in obsessive compulsive disorder (OCD). Ser otonin receptors are certainly positioned to modulate activity within this 'limbic loop', either via 5-HT2A-mediated reductions in striatal dopamine release, 5-HT1D-mediated reductions in pallidal or nigral GAB A release from striatal projection neurons, or via 5-HT3- or 5-HT1A-me diated 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 poss ible basis of neuronal dysfunction in OCD.