Abstract
SummaryEvidence 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-HT2A-mediated reductions in striatal dopamine release, 5-HT1D-mediated reductions in pallidal or nigral GABA release from striatal projection neurons, or via 5-HT3- or 5-HT1A-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.
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