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@ARTICLE{Cremer:5513,
      author       = {Cremer, C.M. and Palomero-Gallagher, N. and Bidmon, H.-J.
                      and Schleicher, A. and Speckmann, E.-J. and Zilles, K.},
      title        = {{P}entylenetetrazole-induced seizures affect binding site
                      densities for {GABA}, glutamate and adenosine receptors in
                      the rat brain},
      journal      = {Neuroscience},
      volume       = {163},
      issn         = {0306-4522},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {PreJuSER-5513},
      pages        = {490 - 499},
      year         = {2009},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {Pentylenetetrazole (PTZ) is a convulsant used to model
                      epileptic seizures in rats. In the PTZ-model, altered heat
                      shock protein 27 (HSP-27) expression highlights
                      seizure-affected astrocytes, which play an important role in
                      glutamate and GABA metabolism. This raises the question
                      whether impaired neurotransmitter metabolism leads to an
                      imbalance in neurotransmitter receptor expression.
                      Consequently, we investigated the effects of seizures on the
                      densities of seven different neurotransmitter receptors in
                      rats which were repeatedly treated with PTZ (40 mg/kg) over
                      a period of 14 days. Quantitative in vitro receptor
                      autoradiography was used to measure the regional binding
                      site densities of the glutamate
                      alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid
                      (AMPA), kainate and N-methyl-D-aspartate (NMDA) receptors,
                      the adenosine receptor type 1 (A(1)), which is part of the
                      system controlling glutamate release, and the
                      gamma-aminobutyric acid (GABA) receptors GABA(A) and GABA(B)
                      as well as the GABA(A)-associated benzodiazepine (BZ)
                      binding sites in each rat. Our results demonstrate altered
                      receptor densities in brain regions of PTZ-treated animals,
                      including the HSP-27 expressing foci (i.e. amygdala,
                      piriform and entorhinal cortex, dentate gyrus). A general
                      decrease of kainate receptor densities was observed together
                      with an increase of NMDA binding sites in the hippocampus,
                      the somatosensory, piriform and the entorhinal cortices.
                      Furthermore, A(1) binding sites were decreased in the
                      amygdala and hippocampal CA1 region (CA1), while BZ binding
                      sites were increased in the dentate gyrus and CA1. Our data
                      demonstrate the impact of PTZ induced seizures on the
                      densities of kainate, NMDA, A(1) and BZ binding sites in
                      epileptic brain. These changes are not restricted to regions
                      showing glial impairment. Thus, an altered balance between
                      different excitatory (NMDA) and modulatory receptors (A(1),
                      BZ binding sites, kainate) shows a much wider regional
                      distribution than that of glial HSP-27 expression,
                      indicating that receptor changes are not following the glial
                      stress responses, but may precede the HSP-27 expression.},
      keywords     = {Animals / Binding Sites: drug effects / Binding Sites:
                      physiology / Binding, Competitive: drug effects / Binding,
                      Competitive: physiology / Brain: anatomy $\&$ histology /
                      Brain: metabolism / Brain: physiopathology / Convulsants:
                      pharmacology / Disease Models, Animal / Epilepsy: chemically
                      induced / Epilepsy: metabolism / Epilepsy: physiopathology /
                      HSP27 Heat-Shock Proteins: drug effects / HSP27 Heat-Shock
                      Proteins: metabolism / Male / Neuroglia: metabolism /
                      Pentylenetetrazole: pharmacology / Rats / Rats, Wistar /
                      Receptor, Adenosine A1: drug effects / Receptor, Adenosine
                      A1: metabolism / Receptors, AMPA: drug effects / Receptors,
                      AMPA: metabolism / Receptors, GABA: metabolism / Receptors,
                      GABA-A: drug effects / Receptors, GABA-A: metabolism /
                      Receptors, GABA-B: drug effects / Receptors, GABA-B:
                      metabolism / Receptors, Glutamate: metabolism / Receptors,
                      Kainic Acid: drug effects / Receptors, Kainic Acid:
                      metabolism / Receptors, N-Methyl-D-Aspartate: drug effects /
                      Receptors, N-Methyl-D-Aspartate: metabolism / Receptors,
                      Purinergic P1: metabolism / Stress, Physiological:
                      physiology / Synaptic Transmission: drug effects / Synaptic
                      Transmission: physiology / Convulsants (NLM Chemicals) /
                      HSP27 Heat-Shock Proteins (NLM Chemicals) / Hspb1 protein,
                      rat (NLM Chemicals) / Receptor, Adenosine A1 (NLM Chemicals)
                      / Receptors, AMPA (NLM Chemicals) / Receptors, GABA (NLM
                      Chemicals) / Receptors, GABA-A (NLM Chemicals) / Receptors,
                      GABA-B (NLM Chemicals) / Receptors, Glutamate (NLM
                      Chemicals) / Receptors, Kainic Acid (NLM Chemicals) /
                      Receptors, N-Methyl-D-Aspartate (NLM Chemicals) / Receptors,
                      Purinergic P1 (NLM Chemicals) / Pentylenetetrazole (NLM
                      Chemicals) / J (WoSType)},
      cin          = {INM-2 / JARA-BRAIN},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-2-20090406 / $I:(DE-82)080010_20140620$},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19345722},
      UT           = {WOS:000269404600044},
      doi          = {10.1016/j.neuroscience.2009.03.068},
      url          = {https://juser.fz-juelich.de/record/5513},
}