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Journal of Pharmacology And Experimental Therapeutics Fast Forward
First published on September 28, 2005; DOI: 10.1124/jpet.105.091199

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Received for publication June 20, 2005.
Revised September 26, 2005.
Accepted for publication September 27, 2005.

Ketamine produces lasting disruptions in encoding of sensory stimuli

Christina R. Maxwell 1, Richard S Ehrlichman 1, Yuling Liang 1, Danielle Trief 1, Stephen J. Kanes 1, Jonathan Karp 2, Steven J. Siegel 1*

1 University of Pennsylvania 2 Rider University

* Address correspondence to: E-mail: siegels{at}mail.med.upenn.edu

Abstract

The current study analyzed the acute, chronic and lasting effects of ketamine administration in four inbred mouse strains (C3H/He, C57BL/6, FVB, DBA/2) 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 to 1. Examination of multiple phases of auditory processing using auditory evoked potentials (AEP) following acute ketamine (0, 5, 20 mg/kg) treatment revealed C3H mice to be most vulnerable to ketamine-induced alterations in AEP whereas FVB mice exhibited the least electrophysiological sensitivity to ketamine. Overall, the pre-cortical P1 evoked potential component increased in amplitude and latency while 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 but elevated hippocampus epinephrine levels in FVB, 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 AEP were examined among C3H (sensitive) and FVB (insensitive) mice. We observed a decrement of the N1 amplitude that persisted at least one 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 mice. Implications for both ketamine abuse and NMDA hypofunction models of schizophrenia are discussed.


Key words: Ketamine, NMDA receptor, abuse, auditory, evoked, schizophrenia


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