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Article ; Online: Increases of Calbindin-Containing Chandelier Cartridges in Schizophrenia: Fact or Artifact?

Benes, Francine M

2017 Volume 82, Issue 1, Page(s) 4–5

Language	English
Publishing date	2017-07-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2017.05.004
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Article ; Online: The GABA system in schizophrenia: cells, molecules and microcircuitry.

Benes, Francine M

Schizophrenia research

2015 Volume 167, Issue 1-3, Page(s) 1–3

Abstract: This is an overview of several papers that have been published in the Special Issue of Schizophrenia Research entitled The GABA System in Schizophrenia: Cells, Molecules and Microcircuitry. This issue presents a broad range of original reports and ... ...

Abstract	This is an overview of several papers that have been published in the Special Issue of Schizophrenia Research entitled The GABA System in Schizophrenia: Cells, Molecules and Microcircuitry. This issue presents a broad range of original reports and scholarly reviews regarding recent progress in studies of neural circuitry in corticolimbic brain regions in patients with schizophrenia.
MeSH term(s)	Brain/metabolism ; Humans ; Nerve Net/metabolism ; Schizophrenia/genetics ; Schizophrenia/metabolism ; Schizophrenia/pathology ; gamma-Aminobutyric Acid/genetics ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2015-09
Publishing country	Netherlands
Document type	Editorial
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2015.07.017
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Zs.A 2351: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 543: Show issues

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Article ; Online: Building models for postmortem abnormalities in hippocampus of schizophrenics.

Benes, Francine M

Schizophrenia research

2015 Volume 167, Issue 1-3, Page(s) 73–83

Abstract: Postmortem studies have suggested that there is abnormal GABAergic activity in the hippocampus in schizophrenia (SZ). In micro-dissected human hippocampal slices, a loss of interneurons and a compensatory upregulation of GABAA receptor binding activity ... ...

Abstract	Postmortem studies have suggested that there is abnormal GABAergic activity in the hippocampus in schizophrenia (SZ). In micro-dissected human hippocampal slices, a loss of interneurons and a compensatory upregulation of GABAA receptor binding activity on interneurons, but not PNs, has suggested that disinhibitory GABA-to-GABA connections are abnormal in stratum oriens (SO) of CA3/2, but not CA1, in schizophrenia. Abnormal expression changes in the expression of kainate receptor (KAR) subunits 5, 6 and 7, as well as an inwardly-rectifying hyperpolarization-activated cationic channel (Ih3; HCN3) may play important roles in regulating GABA cell activity at the SO CA3/2 locus. The exclusive neurons at this site are GABAergic interneurons; these cells also receive direct projections from the basolateral amygdala (BLA). When the BLA is stimulated by stereotaxic infusion of picrotoxin in rats, KARs influence axodendritic and presynaptic inhibitory mechanisms that regulate both inhibitory and disinhibitory interneurons in the SO-CA3/2 locus. The rat model described here was specifically developed to extend our understanding of these and other postmortem findings and has suggested that GABAergic abnormalities and possible disturbances in oscillatory rhythms may be related to a dysfunction of disinhibitory interneurons at the SO-CA3/2 site of schizophrenics.
MeSH term(s)	Action Potentials/physiology ; Animals ; Disease Models, Animal ; Hippocampus/pathology ; Humans ; Interneurons/pathology ; Interneurons/physiology ; Models, Neurological ; Neural Pathways/pathology ; Postmortem Changes ; Rats ; Schizophrenia/pathology ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2015-09
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2015.01.014
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Article: The neurobiology of bipolar disorder: from circuits to cells to molecular regulation.

Benes, Francine M

Current topics in behavioral neurosciences

2014 Volume 5, Page(s) 127–138

Abstract: Over the past 15 years, postmortem studies of the corticolimbic system in subjects with bipolar disorder (BPD) have demonstrated a variety of abnormalities affecting the gamma aminobutyric acid (GABA)ergic system. Although some of the changes are similar ...

Abstract	Over the past 15 years, postmortem studies of the corticolimbic system in subjects with bipolar disorder (BPD) have demonstrated a variety of abnormalities affecting the gamma aminobutyric acid (GABA)ergic system. Although some of the changes are similar to those seen in individuals with schizophrenia, there are pronounced differences in the regulation of complex networks of genes involved in the expression of GAD67, a key marker for functionally differentiated GABAergic interneurons. Overall, these changes vary not only according to diagnosis, but also subregion and layer, suggesting that the activity of GABA cells in complex neural circuits are differentially affected by the unique extrinsic and intrinsic inputs that they receive at different points along a circuit like the trisynaptic pathway. Our ability to understand the functional implications in terms of complex molecular changes will ultimately influence our ability to develop novel treatments for BPD.
MeSH term(s)	Biomarkers ; Bipolar Disorder/metabolism ; Bipolar Disorder/pathology ; Humans ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Biomarkers ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2014-09-18
Publishing country	Germany
Document type	Journal Article
ISSN	1866-3370
ISSN	1866-3370
DOI	10.1007/7854_2010_75
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Article ; Online: A new paradigm for understanding gamma-aminobutyric acid cell pathology in schizophrenia?

Benes, Francine M

Biological psychiatry

2012 Volume 72, Issue 9, Page(s) 712–713

MeSH term(s)	Female ; Frontal Lobe/metabolism ; GABAergic Neurons/metabolism ; Humans ; Male ; Nerve Fibers, Myelinated/metabolism ; Schizophrenia/metabolism
Language	English
Publishing date	2012-11-01
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2012.09.003
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Article: Nicotinic receptors and functional regulation of GABA cell microcircuitry in bipolar disorder and schizophrenia.

Benes, Francine M

Handbook of experimental pharmacology

2012 , Issue 213, Page(s) 401–417

Abstract: Studies of the hippocampus in postmortem brains from patients with schizophrenia and bipolar disorder have provided evidence for a defect of GABAergic interneurons. Significant decreases in the expression of GAD67, a marker for GABA cell function, have ... ...

Abstract	Studies of the hippocampus in postmortem brains from patients with schizophrenia and bipolar disorder have provided evidence for a defect of GABAergic interneurons. Significant decreases in the expression of GAD67, a marker for GABA cell function, have been found repeatedly in several different brain regions that include the hippocampus. In this region, nicotinic receptors are thought to play an important role in modulating the activity of GABAergic interneurons by influences of excitatory cholinergic afferents on their activity. In bipolar disorder, this influence appears to be particularly prominent in the stratum oriens of sectors CA3/2 and CA1, two sites where these cells constitute the exclusive neuronal cell type. In sector CA3/2, this layer receives a robust excitatory projection from the basolateral amygdala (BLA) and this is thought to play a central role in regulating GABA cells at this locus. Using laser microdissection, recent studies have focused selectively on these two layers and their associated GABA cells using microarray technology. The results have provided support for the idea that nicotinic cholinergic receptors play a particularly important role in regulating the activity of GABA neurons at these loci by regulating the progression of cell cycle and the repair of damaged DNA. In bipolar disorder, there is a prominent reduction in the expression of mRNAs for several different nicotinic subunit isoforms. These decreases could reflect a diminished influence of this receptor system on these GABA cells, particularly in sector CA3/2 where a preponderance of abnormalities have been observed in postmortem studies. In patients with bipolar disorder, excitatory nicotinic cholinergic fibers from the medial septum may converge with glutamatergic fibers from the BLA on GABAergic interneurons in the stratum oriens of CA3/2 and result in disturbances of their genomic and functional integrity, ones that may induce disruptions of the integration of microcircuitry within this region.
MeSH term(s)	Bipolar Disorder/physiopathology ; Glutamate Decarboxylase/physiology ; Hippocampus/physiology ; Humans ; Interneurons/physiology ; Neurons, Afferent/physiology ; Receptors, Nicotinic/physiology ; Schizophrenia/physiopathology ; gamma-Aminobutyric Acid/physiology
Chemical Substances	Receptors, Nicotinic ; gamma-Aminobutyric Acid (56-12-2) ; Glutamate Decarboxylase (EC 4.1.1.15) ; glutamate decarboxylase 1 (EC 4.1.1.15)
Language	English
Publishing date	2012
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/978-3-642-25758-2_13
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Article ; Online: Regulation of cell cycle and DNA repair in post-mitotic GABA neurons in psychotic disorders.

Benes, Francine M

Neuropharmacology

2011 Volume 60, Issue 7-8, Page(s) 1232–1242

Abstract: Disturbances of cell cycle regulation and DNA repair in post-mitotic neurons have been implicated in degenerative and malignant diseases of the human brain. Recent work is now suggesting that abnormal regulation of these functions in GABA cells of the ... ...

Abstract	Disturbances of cell cycle regulation and DNA repair in post-mitotic neurons have been implicated in degenerative and malignant diseases of the human brain. Recent work is now suggesting that abnormal regulation of these functions in GABA cells of the adult hippocampus may also play a role in two neuropsychiatric disorders. In schizophrenia and bipolar disorder, a network of genes involved in the regulation of GAD₆₇, a marker for the functional differentiation of GABA cells, show pronounced changes in expression and include kainate receptor subunits, TGFβ and Wnt signaling pathways, epigenetic factors and transcription factors. One of these genes, cyclin D2, is involved in the regulation of cell cycle and DNA repair and appears to be a pivotal element in linking GAD₆₇ expression with these functional clusters of genes. Dysfunction of post-mitotic GABAergic neurons in the adult hippocampus of patients with psychotic disorders is associated with changes in the expression of genes that are involved in the maintenance of functional and genomic integrity of GABA cells. The nature of these changes is quite different in schizophrenia and bipolar disorder, suggesting that a common cell phenotype (in this case, decreased GAD₆₇ expression) may involve two fundamentally different molecular endophenotypes and reflect unique susceptibility genes involved in the respective disorders. This article is part of a Special Issue entitled 'Trends in neuropharmacology: in memory of Erminio Costa'.
MeSH term(s)	Adult ; Cell Cycle/genetics ; Cell Cycle/physiology ; DNA Repair/physiology ; Glutamate Decarboxylase/metabolism ; Humans ; Neurons/metabolism ; Neurons/pathology ; Neurons/physiology ; Psychotic Disorders/genetics ; Psychotic Disorders/metabolism ; Psychotic Disorders/physiopathology ; Signal Transduction/genetics ; Signal Transduction/physiology ; Transcription Factors/genetics ; Transcription Factors/physiology ; gamma-Aminobutyric Acid/genetics ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	Transcription Factors ; gamma-Aminobutyric Acid (56-12-2) ; Glutamate Decarboxylase (EC 4.1.1.15) ; glutamate decarboxylase 1 (EC 4.1.1.15)
Language	English
Publishing date	2011-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/j.neuropharm.2010.12.011
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Article ; Online: Relationship of GAD(67) regulation to cell cycle and DNA repair in GABA neurons in the adult hippocampus: bipolar disorder versus schizophrenia.

Benes, Francine M

Cell cycle (Georgetown, Tex.)

2010 Volume 9, Issue 4, Page(s) 625–627

MeSH term(s)	Bipolar Disorder/enzymology ; Bipolar Disorder/genetics ; Bipolar Disorder/metabolism ; Cell Cycle ; DNA Repair ; Gene Expression Regulation ; Glutamate Decarboxylase/metabolism ; Hippocampus/cytology ; Hippocampus/enzymology ; Hippocampus/metabolism ; Humans ; Neurons/enzymology ; Neurons/metabolism ; Schizophrenia/enzymology ; Schizophrenia/genetics ; Schizophrenia/metabolism ; gamma-Aminobutyric Acid/metabolism
Chemical Substances	gamma-Aminobutyric Acid (56-12-2) ; Glutamate Decarboxylase (EC 4.1.1.15)
Language	English
Publishing date	2010-02-02
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.9.4.10820
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Article ; Online: Neural circuitry models of schizophrenia: is it dopamine, GABA, glutamate, or something else?

Benes, Francine M

Biological psychiatry

2009 Volume 65, Issue 12, Page(s) 1003–1005

MeSH term(s)	Brain/physiopathology ; Dopamine/physiology ; Glutamic Acid/physiology ; Humans ; Neural Pathways/physiopathology ; Neurons/physiology ; Schizophrenia/physiopathology ; gamma-Aminobutyric Acid/physiology
Chemical Substances	Glutamic Acid (3KX376GY7L) ; gamma-Aminobutyric Acid (56-12-2) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2009-06-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	209434-4
ISSN	1873-2402 ; 0006-3223
ISSN (online)	1873-2402
ISSN	0006-3223
DOI	10.1016/j.biopsych.2009.04.006
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Article: Variability of DNA Methylation within Schizophrenia Risk Loci across Subregions of Human Hippocampus.

Ruzicka, W Brad / Subburaju, Sivan / Benes, Francine M

Genes

2017 Volume 8, Issue 5

Abstract: Identification of 108 genomic regions significantly associated with schizophrenia risk by the Psychiatric Genomics Consortium was a milestone for the field, and much work is now focused on determining the mechanism of risk associated with each locus. ... ...

Abstract	Identification of 108 genomic regions significantly associated with schizophrenia risk by the Psychiatric Genomics Consortium was a milestone for the field, and much work is now focused on determining the mechanism of risk associated with each locus. Within these regions, we investigated variability of DNA methylation, a low-level cellular phenotype closely linked to genotype, in two highly similar cellular populations sampled from the human hippocampus, to draw inferences about the elaboration of genotype to phenotype within these loci enriched for schizophrenia risk. DNA methylation was assessed with the Illumina HumanMethylation450 BeadArray in tissue laser-microdissected from the stratum oriens of subfield CA1 or CA2/3, regions having unique connectivity with intrinsic and extrinsic fiber systems within the hippocampus. Samples consisted of postmortem human hippocampus tissue from eight schizophrenia patients, eight bipolar disorder patients, and eight healthy control subjects. Within these genomic regions, we observed far greater difference in methylation patterns between circuit locations within subjects than in a single subregion between subjects across diagnostic groups, demonstrating the complexity of genotype to phenotype elaboration across the diverse circuitry of the human brain.
Language	English
Publishing date	2017-05-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes8050143
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