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@ARTICLE{Lange:141303,
      author       = {Lange, Maren D and Jüngling, Kay and Paulukat, Linda and
                      Vieler, Marc and Gaburro, Stefano and Sosulina, Liudmila and
                      Blaesse, Peter and Sreepathi, Hari K and Ferraguti,
                      Francesco and Pape, Hans-Christian},
      title        = {{G}lutamic acid decarboxylase 65: a link between
                      {GABA}ergic synaptic plasticity in the lateral amygdala and
                      conditioned fear generalization.},
      journal      = {Neuropsychopharmacology},
      volume       = {39},
      number       = {9},
      issn         = {0893-133X},
      address      = {Basingstoke},
      publisher    = {Nature Publishing Group71819},
      reportid     = {DZNE-2020-07625},
      pages        = {2211-2220},
      year         = {2014},
      abstract     = {An imbalance of the gamma-aminobutyric acid (GABA) system
                      is considered a major neurobiological pathomechanism of
                      anxiety, and the amygdala is a key brain region involved.
                      Reduced GABA levels have been found in anxiety patients, and
                      genetic variations of glutamic acid decarboxylase (GAD), the
                      rate-limiting enzyme of GABA synthesis, have been associated
                      with anxiety phenotypes in both humans and mice. These
                      findings prompted us to hypothesize that a deficiency of
                      GAD65, the GAD isoform controlling the availability of GABA
                      as a transmitter, affects synaptic transmission and
                      plasticity in the lateral amygdala (LA), and thereby
                      interferes with fear responsiveness. Results indicate that
                      genetically determined GAD65 deficiency in mice is
                      associated with (1) increased synaptic length and release at
                      GABAergic connections, (2) impaired efficacy of GABAergic
                      synaptic transmission and plasticity, and (3) reduced
                      spillover of GABA to presynaptic GABAB receptors, resulting
                      in a loss of the associative nature of long-term synaptic
                      plasticity at cortical inputs to LA principal neurons. (4)
                      In addition, training with high shock intensities in
                      wild-type mice mimicked the phenotype of GAD65 deficiency at
                      both the behavioral and synaptic level, indicated by
                      generalization of conditioned fear and a loss of the
                      associative nature of synaptic plasticity in the LA. In
                      conclusion, GAD65 is required for efficient GABAergic
                      synaptic transmission and plasticity, and for maintaining
                      extracellular GABA at a level needed for associative
                      plasticity at cortical inputs in the LA, which, if
                      disturbed, results in an impairment of the cue specificity
                      of conditioned fear responses typifying anxiety disorders.},
      keywords     = {Amygdala: cytology / Amygdala: enzymology / Animals /
                      Association Learning: physiology / Conditioning,
                      Psychological: physiology / Electroshock / Extracellular
                      Space: metabolism / Fear: physiology / Generalization,
                      Psychological: physiology / Glutamate Decarboxylase:
                      genetics / Glutamate Decarboxylase: metabolism / Glutamic
                      Acid: metabolism / Interneurons: cytology / Interneurons:
                      physiology / Long-Term Potentiation: physiology / Male /
                      Mice, Inbred C57BL / Mice, Knockout / Neurons: cytology /
                      Neurons: physiology / Receptors, GABA-B: metabolism /
                      Synaptic Transmission: physiology / gamma-Aminobutyric Acid:
                      metabolism / Receptors, GABA-B (NLM Chemicals) / Glutamic
                      Acid (NLM Chemicals) / gamma-Aminobutyric Acid (NLM
                      Chemicals) / Glutamate Decarboxylase (NLM Chemicals) /
                      glutamate decarboxylase 2 (NLM Chemicals)},
      cin          = {AG Remy},
      ddc          = {610},
      cid          = {I:(DE-2719)1013006},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:24663011},
      pmc          = {pmc:PMC4104340},
      doi          = {10.1038/npp.2014.72},
      url          = {https://pub.dzne.de/record/141303},
}