Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Mark J Niciu; Ioline D Henter; Gerard Sanacora; Carlos A Zarate

doi:10.3109/15622975.2013.829585

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Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Journal article

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Peer reviewed

Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?

Mark J Niciu, Ioline D Henter, Gerard Sanacora and Carlos A Zarate

The world journal of biological psychiatry, Vol.15(1), pp.2-16

01/01/2014

DOI: 10.3109/15622975.2013.829585

PMCID: PMC4180366

PMID: 24024876

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Abstract

Objectives. Preclinical and clinical research in neuropsychiatric disorders, particularly mood and substance use disorders, have historically focused on neurons; however, glial cells-astrocytes, microglia, and oligodendrocytes - also play key roles in these disorders. Methods. Peer-reviewed PubMed/Medline articles published through December 2012 were identified using the following keyword combinations: glia, astrocytes, oligodendrocytes/glia, microglia, substance use, substance abuse, substance dependence, alcohol, opiate, opioid, cocaine, psychostimulants, stimulants, and glutamate. Results. Depressive and substance use disorders are highly comorbid, suggesting a common or overlapping aetiology and pathophysiology. Reduced astrocyte cell number occurs in both disorders. Altered glutamate neurotransmission and metabolism - specifically changes in the levels/activity of transporters, receptors, and synaptic proteins potentially related to synaptic physiology - appear to be salient features of both disorders. Glial cell pathology may also underlie the pathophysiology of both disorders via impaired astrocytic production of neurotrophic factors. Microglial/neuroinflammatory pathology is also evident in both depressive and substance use disorders. Finally, oligodendrocyte impairment decreases myelination and impairs expression of myelin-related genes in both substance use and depressive disorders. Conclusions. Glial-mediated glutamatergic dysfunction is a common neuropathological pathway in both substance use and depression. Therefore, glutamatergic neuromodulation is a rational drug target in this comorbidity.

depression

Glia

drug use disorders

glutamate

alcohol use disorders

Details

Title: Subtitle: Glial abnormalities in substance use disorders and depression: Does shared glutamatergic dysfunction contribute to comorbidity?
Creators: Mark J Niciu - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health
Ioline D Henter - Molecular Imaging Branch, National Institute of Mental Health
Gerard Sanacora - Yale University Department of Psychiatry/Connecticut Mental Health Center (CMHC), Clinical Neuroscience Research Unit (CNRU)
Carlos A Zarate - Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health
Resource Type: Journal article
Publication Details: The world journal of biological psychiatry, Vol.15(1), pp.2-16
DOI: 10.3109/15622975.2013.829585
PMID: 24024876
PMCID: PMC4180366
NLM abbreviation: World J Biol Psychiatry
ISSN: 1562-2975
eISSN: 1814-1412
Publisher: Taylor & Francis
Language: English
Date published: 01/01/2014
Academic Unit: Psychiatry; Iowa Neuroscience Institute
Record Identifier: 9984004074902771

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