Modeling interneuron dysfunction in Schizophrenia

Martin J. Schmidt, Karoly Mirnics

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?

Original languageEnglish (US)
Pages (from-to)152-158
Number of pages7
JournalDevelopmental Neuroscience
Volume34
Issue number2-3
DOIs
StatePublished - Sep 1 2012

Fingerprint

Interneurons
Schizophrenia
gamma-Aminobutyric Acid
Glutamate Decarboxylase
Rodentia
Protein Isoforms
Gene Expression
Brain
Enzymes
Population

Keywords

  • GAD67
  • Gene expression
  • Interneurons
  • Mouse behavior
  • Schizophrenia

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience

Cite this

Modeling interneuron dysfunction in Schizophrenia. / Schmidt, Martin J.; Mirnics, Karoly.

In: Developmental Neuroscience, Vol. 34, No. 2-3, 01.09.2012, p. 152-158.

Research output: Contribution to journalArticle

Schmidt, Martin J. ; Mirnics, Karoly. / Modeling interneuron dysfunction in Schizophrenia. In: Developmental Neuroscience. 2012 ; Vol. 34, No. 2-3. pp. 152-158.
@article{958071f3c0414500a6f265520bb3b3a7,
title = "Modeling interneuron dysfunction in Schizophrenia",
abstract = "Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1{\%} of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?",
keywords = "GAD67, Gene expression, Interneurons, Mouse behavior, Schizophrenia",
author = "Schmidt, {Martin J.} and Karoly Mirnics",
year = "2012",
month = "9",
day = "1",
doi = "10.1159/000336731",
language = "English (US)",
volume = "34",
pages = "152--158",
journal = "Developmental Neuroscience",
issn = "0378-5866",
publisher = "S. Karger AG",
number = "2-3",

}

TY - JOUR

T1 - Modeling interneuron dysfunction in Schizophrenia

AU - Schmidt, Martin J.

AU - Mirnics, Karoly

PY - 2012/9/1

Y1 - 2012/9/1

N2 - Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?

AB - Schizophrenia is a debilitating neurodevelopmental disorder affecting approximately 1% of the population and imposing a significant burden on society. One of the most replicated and well-established postmortem findings is a deficit in the expression of the gene encoding the 67-kDa isoform of glutamic acid decarboxylase (GAD67), the primary GABA-producing enzyme in the brain. GAD67 is expressed in various classes of interneurons, with vastly different morphological, molecular, and physiological properties. Importantly, GABA system deficits in schizophrenia encompass multiple interneuronal subtypes, raising several important questions. First, do different classes of interneurons regulate different aspects of behavior? Second, can we model cell-type-specific GABAergic deficits in mice, and will the rodent findings translate to human physiology? Finally, will this knowledge open the door to knowledge-based approaches to treat schizophrenia?

KW - GAD67

KW - Gene expression

KW - Interneurons

KW - Mouse behavior

KW - Schizophrenia

UR - http://www.scopus.com/inward/record.url?scp=84866303374&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84866303374&partnerID=8YFLogxK

U2 - 10.1159/000336731

DO - 10.1159/000336731

M3 - Article

C2 - 22571893

AN - SCOPUS:84866303374

VL - 34

SP - 152

EP - 158

JO - Developmental Neuroscience

JF - Developmental Neuroscience

SN - 0378-5866

IS - 2-3

ER -