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@ARTICLE{Haghir:6000,
      author       = {Haghir, H. and Kovac, S. and Speckmann, E.-J. and Zilles,
                      K. and Gorji, A.},
      title        = {{P}atterns of neurotransmitter receptor distributions
                      following cortical spreading depression},
      journal      = {Neuroscience},
      volume       = {163},
      issn         = {0306-4522},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {PreJuSER-6000},
      pages        = {1340 - 1352},
      year         = {2009},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {Spreading depression (SD), a self-propagating
                      depolarization of neurons and glia, is believed to play a
                      role in different neurological disorders including migraine
                      aura and acute brain ischaemia. Initiation and propagation
                      of SD modulate excitability of neuronal network. A brief
                      period of excitation heralds SD which is immediately
                      followed first by prolonged nerve cell depression and later
                      by an excitatory phase. The aim of the present study was to
                      characterize local and remote transmitter receptor changes
                      after propagation of cortical SD. Quantitative receptor
                      autoradiography was used to asses 16 transmitter receptor
                      types in combined striatum-hippocampus-cortex slices of the
                      rat 1 h after induction of cortical SD. In neocortical
                      tissues, local increases of glutamate NMDA, AMPA, and
                      kainate receptor binding sites were observed. In addition to
                      up-regulation of ionotropic glutamate receptors, receptor
                      binding sites of GABA(A), muscarinic M1 and M2, adrenergic
                      alpha(1) and alpha(2), and serotonergic 5-HT(2) receptors
                      were increased in the hippocampus. Cortical SD also
                      upregulated NMDA, AMPA, kainate, GABA(A), serotonergic
                      5-HT(2), adrenergic alpha(2) and dopaminergic D1 receptor
                      binding sites in the striatum. These findings indicate
                      selective changes in several receptors binding sites both in
                      cortical and subcortical regions by SD which may explain
                      delayed excitatory phase after SD. Mapping of receptor
                      changes by cortical SD increases our understanding of the
                      mechanism of SD action in associated neurological
                      disorders.},
      keywords     = {Animals / Autoradiography / Cerebral Cortex: physiology /
                      Corpus Striatum: physiology / Cortical Spreading Depression:
                      physiology / Hippocampus: physiology / Microelectrodes /
                      Neuronal Plasticity: physiology / Rats / Receptors,
                      Neurotransmitter: metabolism / Receptors, Neurotransmitter
                      (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:19665048},
      UT           = {WOS:000271690200037},
      doi          = {10.1016/j.neuroscience.2009.07.067},
      url          = {https://juser.fz-juelich.de/record/6000},
}