Journal article
Effects of chronic olanzapine and haloperidol differ on the mouse NI auditory evoked potential
Neuropsychopharmacology (New York, N.Y.), Vol.29(4), pp.739-746
2004
DOI: 10.1038/sj.npp.1300376
Abstract
Auditory evoked potentials have been used in a variety of animal models to assess information-processing impairments in schizophrenia. Previous mouse models have primarily employed a paired click paradigm to assess the transient measures of auditory gating. The current study uses stimulus trains at varied interstimulus intervals (ISI) between 0.25 and 8 s in mice to assess the effects of chronic olanzapine and haloperidol on auditory processing. Data indicate that olanzapine increases the amplitude of the N40, P80, and P20/N40 components of the auditory evoked potential, whereas haloperidol had no such effect. The ISI paradigm also allowed for an evaluation of several components of the mouse evoked potential to assess those that display response properties similar to the human P50 and N100. Data suggest that the mouse N40 displays an ISI response relationship that shares characteristics with the human N100, whereas the P20 appears more consistent with the human P50 across the ISI range evaluated in this task. This study suggests that olanzapine may help improve N100 impairments seen in schizophrenia, while haloperidol does not.
Details
- Title: Subtitle
- Effects of chronic olanzapine and haloperidol differ on the mouse NI auditory evoked potential
- Creators
- Christina R MAXWELL - Division of Neuropsychiatry, Department of Psychiatry, Stanley Center for Experimental Therapeutics in Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesYuling Liang - Division of Neuropsychiatry, Department of Psychiatry, Stanley Center for Experimental Therapeutics in Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesBryanne D WEIGHTMAN - Division of Neuropsychiatry, Department of Psychiatry, Stanley Center for Experimental Therapeutics in Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesStephen J KANES - Division of Neuropsychiatry, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesTed ABEL - Department of Biology, University of Pennsylvania, Philadelphia, PA, United StatesRaquel E GUR - Division of Neuropsychiatry, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesBruce I TURETSKY - Division of Neuropsychiatry, Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, United StatesWarren B BILKER - Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, PA, United StatesRobert H LENOX - Department of Psychiatry, University of Pennsylvania, Philadelphia, PA 19104, United StatesSteven J SIEGEL - Division of Neuropsychiatry, Department of Psychiatry, Stanley Center for Experimental Therapeutics in Psychiatry, University of Pennsylvania, Philadelphia, PA, United States
- Resource Type
- Journal article
- Publication Details
- Neuropsychopharmacology (New York, N.Y.), Vol.29(4), pp.739-746
- DOI
- 10.1038/sj.npp.1300376
- ISSN
- 0893-133X
- eISSN
- 1740-634X
- Publisher
- Nature Publishing; New York, NY
- Language
- English
- Date published
- 2004
- Academic Unit
- Molecular Physiology and Biophysics; Psychiatry; Psychological and Brain Sciences; Iowa Neuroscience Institute; Neuroscience and Pharmacology; Biochemistry and Molecular Biology
- Record Identifier
- 9984065733702771
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