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@ARTICLE{Wedekind:836178,
      author       = {Wedekind, Franziska and Oskamp, Angela and Lang, Markus and
                      Hawlitschka, Alexander and Zilles, Karl and Wree, Andreas
                      and Bauer, Andreas},
      title        = {{I}ntrastriatal administration of botulinum neurotoxin {A}
                      normalizes striatal {D}$_{2}${R} binding and reduces
                      striatal {D}$_{1}${R} binding in male hemiparkinsonian rats},
      journal      = {Journal of neuroscience research},
      volume       = {96},
      number       = {1},
      issn         = {0360-4012},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {FZJ-2017-05301},
      pages        = {75–86},
      year         = {2018},
      abstract     = {Cerebral administration of botulinum neurotoxin A (BoNT-A)
                      has been shown to improve disease-specific motor behavior in
                      a rat model of Parkinson disease (PD). Since the
                      dopaminergic system of the basal ganglia fundamentally
                      contributes to motor function, we investigated the impact of
                      BoNT-A on striatal dopamine receptor expression using in
                      vitro and in vivo imaging techniques (positron emission
                      tomography and quantitative autoradiography, respectively).
                      Seventeen male Wistar rats were unilaterally lesioned with
                      6-hydroxydopamine (6-OHDA) and assigned to two treatment
                      groups 7 weeks later: 10 rats were treated ipsilaterally
                      with an intrastriatal injection of 1 ng BoNT-A, while the
                      others received vehicle (n = 7). All animals were tested
                      for asymmetric motor behavior (apomorphine-induced rotations
                      and forelimb usage) and for striatal expression of dopamine
                      receptors and transporters (D1 R, D2 R, and DAT). The
                      striatal D2 R availability was also quantified
                      longitudinally (1.5, 3, and 5 months after intervention) in
                      5 animals per treatment group. The 6-OHDA lesion alone
                      induced a unilateral PD-like phenotype and a $13\%$ increase
                      of striatal D2 R. BoNT-A treatment reduced the asymmetry in
                      both apomorphine-induced rotational behavior and D2 R
                      expression, with the latter returning to normal values 5
                      months after intervention. D1 R expression was significantly
                      reduced, while DAT concentrations showed no alteration.
                      Independent of the treatment, higher interhemispheric
                      symmetry in raclopride binding to D2 R was generally
                      associated with reduced forelimb akinesia. Our findings
                      indicate that striatal BoNT-A treatment diminishes motor
                      impairment and induces changes in D1 and D2 binding site
                      density in the 6-OHDA rat model of PD.},
      cin          = {INM-2 / INM-1 / INM-5},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-2-20090406 / I:(DE-Juel1)INM-1-20090406 /
                      I:(DE-Juel1)INM-5-20090406},
      pnm          = {571 - Connectivity and Activity (POF3-571)},
      pid          = {G:(DE-HGF)POF3-571},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28695985},
      UT           = {WOS:000425811000009},
      doi          = {10.1002/jnr.24110},
      url          = {https://juser.fz-juelich.de/record/836178},
}