High-dose glycine inhibits the loudness dependence of the auditory evoked potential (LDAEP) in healthy humans |
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Authors: | Barry V O’Neill Rodney J Croft Sumie Leung Chris Oliver K Luan Phan Pradeep J Nathan |
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Institution: | (1) Biological Psychiatry Research Unit, Brain Sciences Institute, Swinburne University of Technology, Melbourne, Australia;(2) Behavioural Neuroscience Laboratory, School of Psychology, Psychiatry, Psychological Medicine, Monash University, Building 17, Clayton, 3800, VIC, Australia;(3) School of Natural and Complementary Medicine, Southern Cross University, Lismore, NSW, Australia;(4) Brain Imaging and Emotions Lab (BIEL) Department of Psychiatry, The University of Chicago, Chicago, IL, USA |
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Abstract: | Rationale The loudness dependence of the auditory evoked Potential (LDAEP) has been suggested to be a putative marker of central serotonin
function, with reported abnormalities in clinical disorders presumed to reflect serotonin dysfunction. Despite considerable
research, very little is known about the LDAEP’s sensitivity to other neurotransmitter systems.
Objectives Given the role of N-methyl-d-aspartate (NMDA) receptors in modulating pyramidal cell activity in cortico-cortico and thalamo-cortical loops, we examined
the effect of targeting the glycine modulatory site of the NMDA receptor with high-dose glycine on the LDAEP in healthy subjects.
Materials and methods The study was a double-blind, placebo-controlled repeated-measures design in which 14 healthy participants were tested under
two acute treatment conditions, placebo and oral glycine (0.8 g/kg). Changes in the amplitude of the N1/P2 at varying intensities
(60, 70, 80, 90, 100 dB) were examined at CZ.
Results Compared to placebo, high-dose glycine induced a weaker LDAEP (a pronounced decrease in the slope of the N1/P2 with increasing
tone loudness; p < 0.02).
Conclusion While the exact mechanism responsible for the effects of glycine on the LDAEP are not known, the findings suggest an inhibitory
effect in the cortex, possibly via activation of NMDA receptors on GABA interneurons or inhibitory glycine receptors. The
findings add to the growing literature exhibiting modulation of the LDAEP by multiple neurochemical systems in addition to
the serotonergic system. |
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Keywords: | Glycine NMDA receptor Glutamate Glycine receptor Loudness dependence auditory-evoked potentials LDAEP Electrophysiology Biological marker Serotonin |
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