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@ARTICLE{PalomeroGallagher:5301,
      author       = {Palomero-Gallagher, N. and Bidmon, H.-J. and Cremer, M. and
                      Schleicher, A. and Kircheis, G. and Reifenberger, G. and
                      Kostopoulos, G. and Häussinger, D. and Zilles, K.},
      title        = {{N}eurotransmitter {R}eceptor {I}mbalances in {M}otor
                      {C}ortex and {B}asal {G}anglia in {H}epatic
                      {E}ncephalopathy},
      journal      = {Cellular physiology and biochemistry},
      volume       = {24},
      issn         = {1015-8987},
      address      = {Basel},
      publisher    = {Karger},
      reportid     = {PreJuSER-5301},
      year         = {2009},
      note         = {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).},
      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.},
      keywords     = {Acetylcholine: metabolism / Adenosine: metabolism / Adult /
                      Aged / Autoradiography / Basal Ganglia: physiopathology /
                      Binding Sites / Case-Control Studies / Dopamine: metabolism
                      / Fatal Outcome / Female / Glutamic Acid: metabolism /
                      Hepatic Encephalopathy: physiopathology / Humans / Liver
                      Cirrhosis: metabolism / Liver Cirrhosis, Alcoholic:
                      metabolism / Male / Middle Aged / Motor Cortex: metabolism /
                      Motor Cortex: physiopathology / Norepinephrine: metabolism /
                      Protein Binding / Receptors, Neurotransmitter: metabolism /
                      Serotonin: metabolism / gamma-Aminobutyric Acid: metabolism
                      / Receptors, Neurotransmitter (NLM Chemicals) / Serotonin
                      (NLM Chemicals) / Norepinephrine (NLM Chemicals) /
                      Acetylcholine (NLM Chemicals) / gamma-Aminobutyric Acid (NLM
                      Chemicals) / Glutamic Acid (NLM Chemicals) / Adenosine (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INM-2 / JARA-BRAIN},
      ddc          = {540},
      cid          = {I:(DE-Juel1)INM-2-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Cell Biology / Physiology},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19710544},
      UT           = {WOS:000268679900018},
      doi          = {10.1159/000233254},
      url          = {https://juser.fz-juelich.de/record/5301},
}