Most SGAs differ from older medications pharmacologically in that serotonin 5HT2 receptor binding exceeds their affinity for dopamine D2 receptors, whereas in FGAs this is generally not the case. Largely for that reason, 5HT2 activity has been suggested as one basis for the lower overall risk of extrapyramidal side effects (EPS) with the atypical drugs compared with FGAs [ 5 ]. Other aspects of SGA pharmacology that correlate with reduced risk of EPS include "loose" D2 receptor binding with rapid dissociation rates [ 6 ] and preferential binding of drugs to receptors in limbic and cortical brain regions rather than striatal areas [ 7 ]. None of these hypotheses has been fully confirmed, and the most important message for the clinician is that the pharmacology of these drugs is complex and likely to result in some variability of side effect risk and pharmacokinetics from patient to patient.
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