Document Type

Poster

Publication Date

2013

Publisher

University of Nevada, Las Vegas; Center for Academic Enrichment and Outreach

Abstract

Schizophrenia is a chronic debilitating brain disorder, which affects approximately one per­cent of the adult population worldwide. The symptoms of schizophrenia are commonly divided into three broad classes: positive symptoms, negative symptoms, and cognitive disturbances (Kay, et al., 1987). The positive symptoms of schizophrenia include hallucinations, delusions, and dis­organized thinking, while the negative symptoms include affective flattening, social withdrawal, and an inability to plan and carry out future activities. The cognitive disturbances exhibited in schizophrenia include deficits in spatial reference and working memory as well as difficulties with focus and attention (Lewis et. al., 2007). Several models have been proposed as to the etiology of schizophrenia, one of which proposes the hypofunction of a discrete class of excitatory receptors (NMDA) on primarily inhibitory circuits in the brain. This change in signaling is argued to give rise to a loss of coordinated network activity throughout the brain resulting in deficits observed in schizophrenia (Figure 1). Data for this model is based on postmortem alterations in inhibitory cir­cuits and the ability of drugs that block the function of the NMDA receptor (NMDA antagonists) to produce deficits similar to those seen in schizophrenia populations (Coyle, 2012). The ability of these NMDA antagonists to produce psychosis similar to what is observed in schizophrenia has led to their extensive use in studying the mechanisms responsible for the disorder. Previous studies in our laboratory have demonstrated the ability of ketamine, an NMDA receptor antago­nist, to produce deficits in rodent’s spatial and emotional learning and memory consistent with observations in schizophrenia populations (Bolton et al., 2012; Sabbagh et al., 2012). In these investigations, it was also shown that ketamine administration was sufficient to induce alterations in inhibitory circuits in the brain that are commonly implicated in schizophrenia (Sabbagh et al., 2013). In the present study, we examined the extent to which the same administration of ketamine produced deficits in rodent’s spatial reference and working memory performance in the radial arm maze task. As working memory deficits are a core pathological feature of schizophrenia, these in­vestigations seek to further the validity of the ketamine model as it relates to the etiological origin of schizophrenia.

Keywords

Delusions; Excitatory amino acids--Receptors; Ketamine; Schizophrenia; Schizophrenia--Etiology; Schizophrenia--Treatment; Schizophrenics

Disciplines

Biological Psychology | Biology | Psychology

Language

English


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