@article{KittelSchneiderKenisScheketal.2012,
  author    = {Kittel-Schneider, Sarah and Kenis, Gunter and Schek, Julia and van den Hove, Daniel and Prickaerts, Jos and Lesch, Klaus-Peter and Steinbusch, Harry and Reif, Andreas},
  title     = {Expression of monoamine transporters, nitric oxide synthase 3, and neurotrophin genes in antidepressant-stimulated astrocytes},
  series = {Frontiers in Psychiatry},
  volume    = {3},
  journal   = {Frontiers in Psychiatry},
  doi       = {10.3389/fpsyt.2012.00033},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-123627},
  pages     = {33},
  year      = {2012},
  abstract  = {Background: There is increasing evidence that glial cells play a role in the pathomechanisms of mood disorders and the mode of action of antidepressant drugs. Methods: To examine whether there is a direct effect on the expression of different genes encoding proteins that have been implicated in the pathophysiology of affective disorders, primary astrocyte cell cultures from rats were treated with two different antidepressant drugs, imipramine and escitalopram, and the RNA expression of brain-derived neurotrophic factor (Bdnf), serotonin transporter (5Htt), dopamine transporter (Dat), and endothelial nitric oxide synthase (Nos3) was examined. Results: Stimulation of astroglial cell culture with imipramine, a tricyclic antidepressant, led to a significant increase of the Bdnf RNA level whereas treatment with escitalopram did not. In contrast, 5Htt was not differentially expressed after antidepressant treatment. Finally, neither Dat nor Nos3 RNA expression was detected in cultured astrocytes. Conclusion: These data provide further evidence for a role of astroglial cells in the molecular mechanisms of action of antidepressants.},
  language  = {en}
}
@article{AlbertWeissenbergerStetterMeuthetal.2012,
  author    = {Albert-Weissenberger, Christiane and Stetter, Christian and Meuth, Sven G. and G{\"o}bel, Kerstin and Bader, Michael and Sir{\´e}n, Anna-Leena and Kleinschnitz, Christoph},
  title     = {Blocking of Bradykinin Receptor B1 Protects from Focal Closed Head Injury in Mice by Reducing Axonal Damage and Astroglia Activation},
  series = {Journal of Cerebral Blood Flow and Metabolism},
  volume    = {32},
  journal   = {Journal of Cerebral Blood Flow and Metabolism},
  number    = {9},
  doi       = {10.1038/jcbfm.2012.62},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125903},
  pages     = {1747-1756},
  year      = {2012},
  abstract  = {The two bradykinin receptors B1R and B2R are central components of the kallikrein-kinin system with different expression kinetics and binding characteristics. Activation of these receptors by kinins triggers inflammatory responses in the target organ and in most situations enhances tissue damage. We could recently show that blocking of B1R, but not B2R, protects from cortical cryolesion by reducing inflammation and edema formation. In the present study, we investigated the role of B1R and B2R in a closed head model of focal traumatic brain injury (TBI; weight drop). Increased expression of B1R in the injured hemispheres of wild-type mice was restricted to the later stages after brain trauma, i.e. day 7 (P<0.05), whereas no significant induction could be observed for the B2R (P>0.05). Mice lacking the B1R, but not the B2R, showed less functional deficits on day 3 (P<0.001) and day 7 (P<0.001) compared with controls. Pharmacological blocking of B1R in wild-type mice had similar effects. Reduced axonal injury and astroglia activation could be identified as underlying mechanisms, while inhibition of B1R had only little influence on the local inflammatory response in this model. Inhibition of B1R may become a novel strategy to counteract trauma-induced neurodegeneration.},
  language  = {en}
}