@article{LischkeHerpertzBergeretal.2017,
  author    = {Lischke, Alexander and Herpertz, Sabine C. and Berger, Christoph and Domes, Gregor and Gamer, Matthias},
  title     = {Divergent effects of oxytocin on (para-)limbic reactivity to emotional and neutral scenes in females with and without borderline personality disorder},
  series = {Social Cognitive and Affective Neuroscience},
  volume    = {12},
  journal   = {Social Cognitive and Affective Neuroscience},
  number    = {11},
  doi       = {10.1093/scan/nsx107},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-173309},
  pages     = {1783-1792},
  year      = {2017},
  abstract  = {Borderline personality disorder (BPD) patients' hypersensitivity for emotionally relevant stimuli has been suggested be due to abnormal activity and connectivity in (para-)limbic and prefrontal brain regions during stimulus processing. The neuropeptide oxytocin has been shown to modulate activity and functional connectivity in these brain regions, thereby optimizing the processing of emotional and neutral stimuli. To investigate whether oxytocin would be capable of attenuating BPD patients' hypersensitivity for such stimuli, we recorded brain activity and gaze behavior during the processing of complex scenes in 51 females with and 48 without BPD after intranasal application of either oxytocin or placebo. We found divergent effects of oxytocin on BPD and healthy control (HC) participants' (para-)limbic reactivity to emotional and neutral scenes: Oxytocin decreased amygdala and insula reactivity in BPD participants but increased it in HC participants, indicating an oxytocin-induced normalization of amygdala and insula activity during scene processing. In addition, oxytocin normalized the abnormal coupling between amygdala activity and gaze behavior across all scenes in BPD participants. Overall, these findings suggest that oxytocin may be capable of attenuating BPD patients' hypersensitivity for complex scenes, irrespective of their valence.},
  language  = {en}
}
@article{GruenewaldLangeWerneretal.2017,
  author    = {Gr{\"u}newald, Benedikt and Lange, Maren D and Werner, Christian and O'Leary, Aet and Weishaupt, Andreas and Popp, Sandy and Pearce, David A and Wiendl, Heinz and Reif, Andreas and Pape, Hans C and Toyka, Klaus V and Sommer, Claudia and Geis, Christian},
  title     = {Defective synaptic transmission causes disease signs in a mouse model of juvenile neuronal ceroid lipofuscinosis},
  series = {eLife},
  volume    = {6},
  journal   = {eLife},
  number    = {e28685},
  doi       = {10.7554/eLife.28685},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-170004},
  year      = {2017},
  abstract  = {Juvenile neuronal ceroid lipofuscinosis (JNCL or Batten disease) caused by mutations in the CLN3 gene is the most prevalent inherited neurodegenerative disease in childhood resulting in widespread central nervous system dysfunction and premature death. The consequences of CLN3 mutation on the progression of the disease, on neuronal transmission, and on central nervous network dysfunction are poorly understood. We used Cln3 knockout (Cln3\(^{Δex1-6}\)) mice and found increased anxiety-related behavior and impaired aversive learning as well as markedly affected motor function including disordered coordination. Patch-clamp and loose-patch recordings revealed severely affected inhibitory and excitatory synaptic transmission in the amygdala, hippocampus, and cerebellar networks. Changes in presynaptic release properties may result from dysfunction of CLN3 protein. Furthermore, loss of calbindin, neuropeptide Y, parvalbumin, and GAD65-positive interneurons in central networks collectively support the hypothesis that degeneration of GABAergic interneurons may be the cause of supraspinal GABAergic disinhibition.},
  language  = {en}
}