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Research ArticleNEUROPHARMACOLOGY

Ketamine Produces Lasting Disruptions in Encoding of Sensory Stimuli

Christina R. Maxwell, Richard S. Ehrlichman, Yuling Liang, Danielle Trief, Stephen J. Kanes, Jonathan Karp and Steven J. Siegel
Journal of Pharmacology and Experimental Therapeutics January 2006, 316 (1) 315-324; DOI: https://doi.org/10.1124/jpet.105.091199
Christina R. Maxwell
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Richard S. Ehrlichman
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Yuling Liang
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Danielle Trief
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Stephen J. Kanes
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Jonathan Karp
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Steven J. Siegel
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Abstract

The current study analyzed the acute, chronic, and lasting effects of ketamine administration in four inbred mouse strains (C3H/HeHsd, C57BL/6Hsd, FVB/Hsd, and DBA/2Hsd) to evaluate vulnerability to ketamine as a drug of abuse and as a model of schizophrenia. Serum half-life of ketamine was similar between all strains (approximately 13 min). Also, the ratio of brain-to-serum ketamine levels was 3:1. Examination of multiple phases of auditory processing using auditory-evoked potentials (AEPs) following acute ketamine (0, 5, and 20 mg/kg) treatment revealed C3H/HeHsd mice to be most vulnerable to ketamine-induced alterations in AEPs, whereas FVB/Hsd mice exhibited the least electrophysiological sensitivity to ketamine. Overall, the precortical P1-evoked potential component increased in amplitude and latency, whereas the cortically generated N1 and P2 components decreased in amplitude and latency following acute ketamine across all strains. Brain catecholamine analyses indicated that ketamine decreased hippocampus epinephrine levels in C3H/HeHsd but elevated hippocampus epinephrine levels in FVB/Hsd, suggesting one potential mechanism for AEP vulnerability to ketamine. Based on results of the acute study, the immediate and lasting effects of chronic low-dose ketamine on AEPs were examined among C3H/HeHsd (sensitive) and FVB/Hsd (insensitive) mice. We observed a decrement of the N1 amplitude that persisted at least 1 week after the last exposure to ketamine across both strains. This lasting deficit in information processing occurred in the absence of acute changes among the FVB/Hsd mice. Implications for both ketamine abuse and N-methyl-d-aspartate hypofunction models of schizophrenia are discussed.

Footnotes

  • This work was supported by funding from the National Institutes of Health/National Institute on Drug Abuse Grant 5-R21-DA-017082-02 (to S.J.S.), the Stanley Medical Research Institute (to S.J.S.), and National Institutes of Health Grant P50-MH6404501 (to S.J.S., S.J.K., and Raquel E. Gur, principal investigator).

  • Article, publication date, and citation information can be found at http://jpet.aspetjournals.org.

  • doi:10.1124/jpet.105.091199.

  • ABBREVIATIONS: AEP, auditory evoked potential; HPLC, high-performance liquid chromatography.

    • Received June 17, 2005.
    • Accepted September 27, 2005.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 316 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 316, Issue 1
1 Jan 2006
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Research ArticleNEUROPHARMACOLOGY

Ketamine Produces Lasting Disruptions in Encoding of Sensory Stimuli

Christina R. Maxwell, Richard S. Ehrlichman, Yuling Liang, Danielle Trief, Stephen J. Kanes, Jonathan Karp and Steven J. Siegel
Journal of Pharmacology and Experimental Therapeutics January 1, 2006, 316 (1) 315-324; DOI: https://doi.org/10.1124/jpet.105.091199

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Research ArticleNEUROPHARMACOLOGY

Ketamine Produces Lasting Disruptions in Encoding of Sensory Stimuli

Christina R. Maxwell, Richard S. Ehrlichman, Yuling Liang, Danielle Trief, Stephen J. Kanes, Jonathan Karp and Steven J. Siegel
Journal of Pharmacology and Experimental Therapeutics January 1, 2006, 316 (1) 315-324; DOI: https://doi.org/10.1124/jpet.105.091199
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