You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 57 No. 1, January 2000 TABLE OF CONTENTS
  Archives
  •  Online Features
  Perspectives
 This Article
 •Full text
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on ISI (57)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Topic Collections
 •Psychiatry, Other
 •Alert me on articles by topic

Mind Glue

Implications of Glial Cell Biology for Psychiatry

Joseph T. Coyle, MD; Robert Schwarcz, PhD

Arch Gen Psychiatry. 2000;57:90-93.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

INTRODUCTION

The legacy of the last century of research in psychiatry has been the sophisticated understanding of the role of neuronal systems in brain function and ultimately in psychopathology. As a consequence, an armamentarium of drugs to treat neuropsychiatric disorders has been developed that work by altering chemical neurotransmission in the brain. Curiously, little attention has been paid to the nonneuronal cellular components of the brain, which outnumber neurons by a factor of 10.1 Glia, a heterogeneous population of cells, have largely been viewed as passive handmaidens to the neurons, which have been considered the primary arbiters of information processing in the brain. The term glia, which means glue in German, was first applied to these cells by Virchow2 in a psychiatric report more than 150 years ago.

Recent research, however, has demonstrated that glia are far from passive but actively participate in . . . [Full Text of this Article]

ASTROGLIA

EXCITATORY NEUROTRANSMISSION

TROPHIC FACTORS

MICROGLIA

STEM CELLS

CONCLUSIONS

From the Department of Psychiatry, Harvard Medical School, Boston, Mass (Dr Coyle); and the Maryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore (Dr Schwarcz).



THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Convergent evidence that oligodendrocyte lineage transcription factor 2 (OLIG2) and interacting genes influence susceptibility to schizophrenia
Georgieva et al.
Proc. Natl. Acad. Sci. USA 2006;103:12469-12474.
ABSTRACT | FULL TEXT  

Does Glial Asthenia Predispose to Schizophrenia?
Moises and Gottesman
Arch Gen Psychiatry 2004;61:1170-1170.
FULL TEXT  

Toward a Rapidly Acting Antidepressant: The Normetanephrine and Extraneuronal Monoamine Transporter (Uptake 2) Hypothesis
Schildkraut and Mooney
Am. J. Psychiatry 2004;161:909-911.
ABSTRACT | FULL TEXT  

Life Stress, Genes, and Depression: Multiple Pathways Lead to Increased Risk and New Opportunities for Intervention
Charney and Manji
Sci Signal 2004;2004:re5-re5.
ABSTRACT | FULL TEXT  

Regional brain chemical alterations in young children with autism spectrum disorder
Friedman et al.
Neurology 2003;60:100-107.
ABSTRACT | FULL TEXT  

The neuropathology of primary mood disorder
Harrison
Brain 2002;125:1428-1449.
ABSTRACT | FULL TEXT  

Reduced Neuronal Size and Glial Cell Density in Area 9 of the Dorsolateral Prefrontal Cortex in Subjects with Major Depressive Disorder
Cotter et al.
Cereb Cortex 2002;12:386-394.
ABSTRACT | FULL TEXT  

Reduced Glial Cell Density and Neuronal Size in the Anterior Cingulate Cortex in Major Depressive Disorder
Cotter et al.
Arch Gen Psychiatry 2001;58:545-553.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2000 American Medical Association. All Rights Reserved.