The association of excitation and inhibition signaling with the relative symptom expression of autism and psychosis-proneness: Implications for psychopharmacology

Talitha C. Ford, Ahmad Abu-Akel, David P. Crewther

Research output: Contribution to journalArticlepeer-review

Abstract

The underlying mechanisms of autism and schizophrenia are poorly understood, partly due to a lack of dimension-specific research. Aberrant excitatory and inhibitory neurotransmission are implicated in both conditions, particularly in social dysfunction. This study investigates the extent to which the degree of autistic tendency and psychosis-proneness exclusively and interactively predict excitatory and inhibitory neurotransmitter concentrations in the superior temporal cortex (STC). In 38 adults (18 male, 18–40 years), we obtained autistic tendencies (Autism-Spectrum Quotient [AQ]) and psychosis-proneness scores (Schizotypal Personality Questionnaire [PP]); magnetic resonance spectroscopy (MRS) quantified glutamate and GABA+ concentrations from the STC. Results demonstrated a negative AQ/PP interaction with glutamate concentration for the left STC voxel, where PP increased with glutamate for average AQ, while AQ decreased with glutamate for average-high PP. There was a negative AQ/PP interaction with glutamate/GABA+ ratio for the right STC, AQ increasing with glutamate/GABA+ for low-average PP, while PP decreased with glutamate/GABA+ for high AQ. Consistent with animal studies, we also reveal that overall reduced glutamate/GABA+ ratio might be precipitated by increased right hemisphere GABA+ concentrations. These findings illustrate the importance of considering the concurrent effects of autism and psychosis dimensions on understanding the pathophysiological mechanisms implicated in either condition, and can advance psychopharmacological research into better treatment options for patients.

Original languageEnglish
Pages (from-to)235-242
Number of pages8
JournalProgress in Neuro-Psychopharmacology and Biological Psychiatry
Volume88
DOIs
StatePublished - 10 Jan 2019
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported by The National Health and Medical Research Council of Australia (APP1004740); Swinburne University Neuroimaging Grant; and a Swinburne University Postgraduate Research Award. These funding bodies had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.

Funding Information:
We thank Swinburne Neuroimaging for their support through data collection and analysis. The authors also acknowledge the facilities of Swinburne Neuroimaging (SNI) and its flagship funding from the National Imaging Facility (NIF) under the National Collaborative Researcher Infrastructure Strategy (NCRIS) implemented by the Australian Government.

Funding Information:
This work was supported by The National Health and Medical Research Council of Australia ( APP1004740 ); Swinburne University Neuroimaging Grant ; and a Swinburne University Postgraduate Research Award . These funding bodies had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.

Publisher Copyright:
© 2018 Elsevier Inc.

Keywords

  • Autism
  • GABA
  • Glutamate
  • MRS
  • Psychosis-proneness

ASJC Scopus subject areas

  • Pharmacology
  • Biological Psychiatry

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