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Olanzapine: a basic science update

Published online by Cambridge University Press:  06 August 2018

Franklin Bymaster*
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
Kenneth W. Perry
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
David L. Nelson
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
David T. Wong
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
Kurt Rasmussen
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
Nick A. Moore
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
David O. Calligaro
Affiliation:
Neuroscience Research Division, Eli Lilly and Company, Indianapolis, IN, USA
*
Correspondence: F. Bymaster, Neuroscience Research Division, Lilly Research Laboratories, Lilly Corporate Center, Indianapolis, IN 46285 0510, USA
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Abstract

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Olanzapine, an atypical antipsychotic, has a broad receptor binding profile, which may account for its pharmacological effects in schizophrenia. In vitro receptor binding studies showed a high affinity for dopamine D2, D3, and D4 receptors; all 5-HT2 receptor subtypes and the 5-HT6 receptor; muscarinic receptors, especially the M1 subtype; and α1-adrenergic receptors. In vivo studies showed that olanzapine had potent activity at D2 and 5 -HT2A receptors, but much less activity at D1 and muscarinic receptors, and that it inhibited dopaminergic neurons in the A10 but not the A9 tract, suggesting that this agent will not cause extrapyramidal side-effects (EPS). Microdialysis studies showed that olanzapine increased the extracellular levels of norepinephrine and dopamine, but not 5-HT, in the prefrontal cortex, and increased extracellular dopamine levels in the neostriatum and nucleus accumbens, areas ofthe brain associated with schizophrenia. Studies of gene expression showed that olanzapine 10 mg/kg also increased Fos expression in the prefrontal cortex, the dorsolateral striatum, and the nucleus accumbens. These findings are consistent with the effectiveness of olanzapine on both negative and positive symptoms and suggest that, with careful dosing, olanzapine should not cause EPS.

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Type
Research Article
Copyright
Copyright © The Royal College of Psychiatrists, 1999 

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