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Table of Contents
Vol. 24, No. 3-4, 2009
Issue release date: August 2009
Section title: Original Paper
Cell Physiol Biochem 2009;24:291–306
(DOI:10.1159/000233254)

Neurotransmitter Receptor Imbalances in Motor Cortex and Basal Ganglia in Hepatic Encephalopathy

Palomero-Gallagher N.1,2 · Bidmon H.-J.3 · Cremer M.1 · Schleicher A.3 · Kircheis G.4 · Reifenberger G.5 · Kostopoulos G.6 · Häussinger D.4 · Zilles K.1,2,3,7
1Institute of Neurosciences and Medicine (INM-2), Research Center Jülich,2JARA - Translational Brain Medicine,3C.&O. Vogt Institute of Brain Research, Heinrich-Heine-University, Düsseldorf,4Clinic for Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-University, Düsseldorf,5Department of Neuropathology, Heinrich-Heine-University, Düsseldorf,6Medical School, University of Patras, Patras,7Brain Imaging Center West, Research Center Jülich, Jülich
email Corresponding Author

Nicola Palomero-Gallagher

Institute of Neurosciences and Medicine (INM-2)

Research Center Jülich, 52425 Jülich (Germany)

Tel. +49-2461 614790, Fax: +49-2461 612820

E-Mail n.palomero-gallagher@fz-juelich.de

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Abstract

Hepatic encephalopathy (HE) in chronic liver disease is characterized by neuropsychiatric and motor disturbances and associated with a net increase of inhibitory neurotransmission. Though many studies, mostly carried out in animal models, have linked dysfunctions of single neurotransmitter systems with the pathogenesis of HE, reports concerning neurotransmitter receptor alterations are controversial. Little is known about the situation in humans. We carried out a multireceptor assessment of HE-associated changes in neurotransmitter receptor densities and affinities in human post-mortem brain samples. Dissociation constants and densities of different binding sites for glutamate, GABA, acetylcholine, norepinephrine, serotonin, dopamine and adenosine were determined by in vitro binding assays and quantitative receptor autoradiography in the motor cortex and putamen of HE and control brains. HE cases do not build a homogeneous group, but differ concerning direction and intensity of binding site density divergences from control values. The acetylcholine M2 binding site dissociation constant was significantly higher in HE brains. Nicotinic acetylcholine and adenosine type 1 and 2A densities were significantly down-regulated in the putamen of HE brains. Our data suggest that neurotransmitter alterations are probably not the primary key factor responsible for the neuropsychiatric and motor disturbances associated with HE.

© 2009 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Accepted: July 02, 2009
Published online: August 03, 2009
Issue release date: August 2009

Number of Print Pages: 16
Number of Figures: 0
Number of Tables: 0

ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)

For additional information: http://www.karger.com/CPB


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