Home > Publications database > Neurotransmitter Receptor Imbalances in Motor Cortex and Basal Ganglia in Hepatic Encephalopathy > print

001     5301
005     20180208224420.0
024 7 _ |2 pmid
|a pmid:19710544
024 7 _ |2 DOI
|a 10.1159/000233254
024 7 _ |2 WOS
|a WOS:000268679900018
037 _ _ |a PreJuSER-5301
041 _ _ |a eng
082 _ _ |a 540
084 _ _ |2 WoS
|a Cell Biology
084 _ _ |2 WoS
|a Physiology
100 1 _ |a Palomero-Gallagher, N.
|b 0
|u FZJ
|0 P:(DE-Juel1)VDB1208
245 _ _ |a Neurotransmitter Receptor Imbalances in Motor Cortex and Basal Ganglia in Hepatic Encephalopathy
260 _ _ |a Basel
|b Karger
|c 2009
300 _ _ |a
336 7 _ |a Journal Article
|0 PUB:(DE-HGF)16
|2 PUB:(DE-HGF)
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|0 0
|2 EndNote
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a article
|2 DRIVER
440 _ 0 |a Cellular Physiology and Biochemistry
|x 1015-8987
|0 21027
|y 3
|v 24
500 _ _ |a The authors thank S. Wilms, S. Krause and A. Borner for excellent technical assistance. This project was supported by the Deutsche Forschungsgemeinschaft through the Sonderforschungsbereich 575 "Experimental Hepatology" (project C5).
520 _ _ |a 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.
536 _ _ |a Funktion und Dysfunktion des Nervensystems
|c P33
|2 G:(DE-HGF)
|0 G:(DE-Juel1)FUEK409
|x 0
588 _ _ |a Dataset connected to Web of Science, Pubmed
650 _ 2 |2 MeSH
|a Acetylcholine: metabolism
650 _ 2 |2 MeSH
|a Adenosine: metabolism
650 _ 2 |2 MeSH
|a Adult
650 _ 2 |2 MeSH
|a Aged
650 _ 2 |2 MeSH
|a Autoradiography
650 _ 2 |2 MeSH
|a Basal Ganglia: physiopathology
650 _ 2 |2 MeSH
|a Binding Sites
650 _ 2 |2 MeSH
|a Case-Control Studies
650 _ 2 |2 MeSH
|a Dopamine: metabolism
650 _ 2 |2 MeSH
|a Fatal Outcome
650 _ 2 |2 MeSH
|a Female
650 _ 2 |2 MeSH
|a Glutamic Acid: metabolism
650 _ 2 |2 MeSH
|a Hepatic Encephalopathy: physiopathology
650 _ 2 |2 MeSH
|a Humans
650 _ 2 |2 MeSH
|a Liver Cirrhosis: metabolism
650 _ 2 |2 MeSH
|a Liver Cirrhosis, Alcoholic: metabolism
650 _ 2 |2 MeSH
|a Male
650 _ 2 |2 MeSH
|a Middle Aged
650 _ 2 |2 MeSH
|a Motor Cortex: metabolism
650 _ 2 |2 MeSH
|a Motor Cortex: physiopathology
650 _ 2 |2 MeSH
|a Norepinephrine: metabolism
650 _ 2 |2 MeSH
|a Protein Binding
650 _ 2 |2 MeSH
|a Receptors, Neurotransmitter: metabolism
650 _ 2 |2 MeSH
|a Serotonin: metabolism
650 _ 2 |2 MeSH
|a gamma-Aminobutyric Acid: metabolism
650 _ 7 |0 0
|2 NLM Chemicals
|a Receptors, Neurotransmitter
650 _ 7 |0 50-67-9
|2 NLM Chemicals
|a Serotonin
650 _ 7 |0 51-41-2
|2 NLM Chemicals
|a Norepinephrine
650 _ 7 |0 51-84-3
|2 NLM Chemicals
|a Acetylcholine
650 _ 7 |0 56-12-2
|2 NLM Chemicals
|a gamma-Aminobutyric Acid
650 _ 7 |0 56-86-0
|2 NLM Chemicals
|a Glutamic Acid
650 _ 7 |0 58-61-7
|2 NLM Chemicals
|a Adenosine
650 _ 7 |a J
|2 WoSType
653 2 0 |2 Author
|a Human post-mortem brain tissue
653 2 0 |2 Author
|a Neurotransmitter receptors
653 2 0 |2 Author
|a Acetylcholine
653 2 0 |2 Author
|a Adenosine
653 2 0 |2 Author
|a Putamen
700 1 _ |a Bidmon, H.-J.
|b 1
|0 P:(DE-HGF)0
700 1 _ |a Cremer, M.
|b 2
|u FZJ
|0 P:(DE-Juel1)VDB21539
700 1 _ |a Schleicher, A.
|b 3
|0 P:(DE-HGF)0
700 1 _ |a Kircheis, G.
|b 4
|0 P:(DE-HGF)0
700 1 _ |a Reifenberger, G.
|b 5
|0 P:(DE-HGF)0
700 1 _ |a Kostopoulos, G.
|b 6
|0 P:(DE-HGF)0
700 1 _ |a Häussinger, D.
|b 7
|0 P:(DE-HGF)0
700 1 _ |a Zilles, K.
|b 8
|u FZJ
|0 P:(DE-Juel1)131714
773 _ _ |a 10.1159/000233254
|g Vol. 24
|q 24
|0 PERI:(DE-600)1482056-0
|t Cellular physiology and biochemistry
|v 24
|y 2009
|x 1015-8987
856 7 _ |u http://dx.doi.org/10.1159/000233254
909 C O |o oai:juser.fz-juelich.de:5301
|p VDB
913 1 _ |k P33
|v Funktion und Dysfunktion des Nervensystems
|l Funktion und Dysfunktion des Nervensystems
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914 1 _ |y 2009
915 _ _ |0 StatID:(DE-HGF)0010
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|l Molekulare Organisation des Gehirns
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920 1 _ |0 I:(DE-82)080010_20140620
|k JARA-BRAIN
|l Jülich-Aachen Research Alliance - Translational Brain Medicine
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