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P-1260 - Neurochemical Modulation of Auditory Processing in Healthy Controls Stratified for low and High Auditory Hallucinatory Experiences

Published online by Cambridge University Press:  15 April 2020

V.J. Knott ,
A.M. Millar ,
J.F. McIntosh ,
D.K. Shah ,
D.J. Fisher ,
C.M. Blais ,
V. Ilivitsky  and
E. Horn
V.J. Knott
Affiliation:
Clinical Neuroelectrophysiology and Cognitive Research Laboratory, University of Ottawa Institute of Mental Health Research, Ottawa, ON, Canada
A.M. Millar
Affiliation:
Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada
J.F. McIntosh
Affiliation:
Institute of Cognitive Science, Carleton University, Ottawa, ON, Canada
D.K. Shah
Affiliation:
Psychiatry, Ottawa, ON, Canada
D.J. Fisher
Affiliation:
Psychology, University of Ottawa, Ottawa, ON, Canada
C.M. Blais
Affiliation:
Psychology, Carleton University, Ottawa, ON, Canada
V. Ilivitsky
Affiliation:
Royal Ottawa Mental Health Centre, Ottawa, ON, Canada
E. Horn
Affiliation:
Royal Ottawa Mental Health Centre, Ottawa, ON, Canada

Abstract

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Introduction

Contributing to poor global functioning, auditory hallucinations (AH) also interfere with elementary cognitive processes, including auditory discrimination. This is evidenced in schizophrenic (SZ) hallucinators (vs. non-hallucinators) by a greater reduction of the MMN, an auditory event-related brain potential (ERP) generated in part by NMDA receptor activity and normalized with nicotinic (nACh) agonist treatment.

Objectives

To increase our understanding of NMDA-nACh interactions with auditory processing, using healthy young adults varying in their degree of experience with AH, thereby reducing the confounding influence of illness chronicity and medication associated with the study of SZ patients.

Aims

To investigate MMN differences between low and high AH subjects during separate and combined administration of ketamine, an NMDA antagonist, and nicotine, an nACh agonist.

Methods

In 40 healthy controls, all rated for AH with the Bell Object Relations and Reality Testing Inventory, MMN to frequency deviants was assessed in a randomized, placebo-controlled crossover design involving the separate and combined administration of a intravenous sub-psychotomimetic dose of ketamine (0.04 mg/kg) and a dose of nicotine gum (4 mg).

Results

In high AH subjects, ketamine reduced MMN, with the resulting amplitude being smaller than that of low AH subjects. This ketamine-induced MMN reduction was evident only with placebo gum; furthermore combined nicotine-ketamine treatment acted to increase MMN in high scorers.

Conclusions

AH in otherwise healthy individuals is associated with heightened sensitivity to NMDA receptor blockade, the effects of which are moderated by nicotinic neurotransmission. Both neurotransmitters may interact to moderate auditory processing and AH in SZ.

Type
Abstract
Information
European Psychiatry , Volume 27 , Issue S1: Abstracts of the 20th European Congress of Psychiatry , 2012 , pp. 1
Copyright
Copyright © European Psychiatric Association 2012
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