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@ARTICLE{Harris:857102,
      author       = {Harris, Nicholas A. and Isaac, Austin T. and Günther, Anne
                      and Merkel, Kevin and Melchior, James and Xu, Michelle and
                      Eguakun, Eghosa and Perez, Rafael and Nabit, Brett P. and
                      Flavin, Stephanie and Gilsbach, Ralf and Shonesy, Brian and
                      Hein, Lutz and Abel, Ted and Baumann, Arnd and Matthews,
                      Robert and Centanni, Samuel W. and Winder, Danny G.},
      title        = {{D}orsal {BNST} α 2{A} -{A}drenergic {R}eceptors {P}roduce
                      {HCN}-{D}ependent {E}xcitatory {A}ctions {T}hat {I}nitiate
                      {A}nxiogenic {B}ehaviors},
      journal      = {The journal of neuroscience},
      volume       = {38},
      number       = {42},
      issn         = {0270-6474},
      address      = {Washington, DC},
      publisher    = {Soc.69657},
      reportid     = {FZJ-2018-06356},
      pages        = {8922-8942},
      year         = {2018},
      abstract     = {Stress is a precipitating agent in neuropsychiatric disease
                      and initiates relapse to drug-seeking behavior in addicted
                      patients. Targeting the stress system in protracted
                      abstinence from drugs of abuse with anxiolytics may be an
                      effective treatment modality for substance use disorders.
                      α2A-adrenergic receptors (α2A-ARs) in extended amygdala
                      structures play key roles in dampening stress responses.
                      Contrary to early thinking, α2A-ARs are expressed at
                      non-noradrenergic sites in the brain. These
                      non-noradrenergic α2A-ARs play important roles in stress
                      responses, but their cellular mechanisms of action are
                      unclear. In humans, the α2A-AR agonist guanfacine reduces
                      overall craving and uncouples craving from stress, yet
                      minimally affects relapse, potentially due to competing
                      actions in the brain. Here, we show that heteroceptor
                      α2A-ARs postsynaptically enhance dorsal bed nucleus of the
                      stria terminalis (dBNST) neuronal activity in mice of both
                      sexes. This effect is mediated by
                      hyperpolarization-activated cyclic nucleotide-gated cation
                      channels because inhibition of these channels is necessary
                      and sufficient for excitatory actions. Finally, this
                      excitatory action is mimicked by clozapine-N-oxide
                      activation of the Gi-coupled DREADD hM4Di in dBNST neurons
                      and its activation elicits anxiety-like behavior in the
                      elevated plus maze. Together, these data provide a framework
                      for elucidating cell-specific actions of GPCR signaling and
                      provide a potential mechanism whereby competing anxiogenic
                      and anxiolytic actions of guanfacine may affect its clinical
                      utility in the treatment of addiction.},
      cin          = {ICS-4},
      ddc          = {610},
      cid          = {I:(DE-Juel1)ICS-4-20110106},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30150361},
      UT           = {WOS:000447587500002},
      doi          = {10.1523/JNEUROSCI.0963-18.2018},
      url          = {https://juser.fz-juelich.de/record/857102},
}