@article{SchaefferKuehnSchmittetal.2013,
  author    = {Schaeffer, Evelin L. and K{\"u}hn, Franziska and Schmitt, Angelika and Gattaz, Wagner F. and Gruber, Oliver and Schneider-Axmann, Thomas and Falkai, Peter and Schmitt, Andrea},
  title     = {Increased cell proliferation in the rat anterior cingulate cortex following neonatal hypoxia: relevance to schizophrenia},
  series = {Journal of Neural Transmission},
  volume    = {120},
  journal   = {Journal of Neural Transmission},
  number    = {1},
  doi       = {10.1007/s00702-012-0859-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-125890},
  pages     = {187-195},
  year      = {2013},
  abstract  = {As a consequence of obstetric complications, neonatal hypoxia has been discussed as an environmental factor in the pathophysiology of schizophrenia. However, the biological consequences of hypoxia are unclear. The neurodevelopmental hypothesis of schizophrenia suggests that the onset of abnormal brain development and neuropathology occurs perinatally, whereas symptoms of the disease appear in early adulthood. In our animal model of chronic neonatal hypoxia, we have detected behavioral alterations resembling those known from schizophrenia. Disturbances in cell proliferation possibly contribute to the pathophysiology of this disease. In the present study, we used postnatal rats to investigate cell proliferation in several brain areas following neonatal hypoxia. Rats were repeatedly exposed to hypoxia (89 \% N2, 11 \% O2) from postnatal day (PD) 4-8. We then evaluated cell proliferation on PD 13 and 39, respectively. These investigations were performed in the anterior cingulate cortex (ACC), caudate-putamen (CPU), dentate gyrus, and subventricular zone. Rats exposed to hypoxia exhibited increased cell proliferation in the ACC at PD 13, normalizing at PD 39. In other brain regions, no alterations have been detected. Additionally, hypoxia-treated rats showed decreased CPU volume at PD 13. The results of the present study on the one hand support the assumption of chronic hypoxia influencing transient cell proliferation in the ACC, and on the other hand reveal normalization during ageing.},
  language  = {en}
}
@article{BoehmeRitterTefikowetal.2015,
  author    = {Boehme, Stephanie and Ritter, Viktoria and Tefikow, Susan and Stangier, Ulrich and Strauss, Bernhard and Miltner, Wolfgang H. R. and Straube, Thomas},
  title     = {Neural correlates of emotional interference in social anxiety disorder},
  series = {PLoS ONE},
  volume    = {10},
  journal   = {PLoS ONE},
  number    = {6},
  doi       = {10.1371/journal.pone.0128608},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-148534},
  pages     = {e0128608},
  year      = {2015},
  abstract  = {Disorder-relevant but task-unrelated stimuli impair cognitive performance in social anxiety disorder (SAD); however, time course and neural correlates of emotional interference are unknown. The present study investigated time course and neural basis of emotional interference in SAD using event-related functional magnetic resonance imaging (fMRI). Patients with SAD and healthy controls performed an emotional stroop task which allowed examining interference effects on the current and the succeeding trial. Reaction time data showed an emotional interference effect in the current trial, but not the succeeding trial, specifically in SAD. FMRI data showed greater activation in the left amygdala, bilateral insula, medial prefrontal cortex (mPFC), dorsal anterior cingulate cortex (ACC), and left opercular part of the inferior frontal gyrus during emotional interference of the current trial in SAD patients. Furthermore, we found a positive correlation between patients' interference scores and activation in the mPFC, dorsal ACC and left angular/supramarginal gyrus. Taken together, results indicate a network of brain regions comprising amygdala, insula, mPFC, ACC, and areas strongly involved in language processing during the processing of task-unrelated threat in SAD. However, specifically the activation in mPFC, dorsal ACC, and left angular/supramarginal gyrus is associated with the strength of the interference effect, suggesting a cognitive network model of attentional bias in SAD. This probably comprises exceeded allocation of attentional resources to disorder-related information of the presented stimuli and increased self-referential and semantic processing of threat words in SAD.},
  language  = {en}
}