@phdthesis{Theisen2013,
  author    = {Theisen, Nina Fee},
  title     = {Einfluss von Atomoxetin und Methylphenidat auf Inhibition und fr{\"u}he Filterprozesse - Eine EEG-Untersuchung bei adulten ADHS-Patienten},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-79543},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Methodik: F{\"u}r diese Studie wurden 34 Patienten zu drei verschiedenen Zeitpunkten untersucht. Hierbei wurden die EEG-Potentiale w{\"a}hrend einer CPT-OX-Testung abgeleitet. F{\"u}r die vorliegende Arbeit sollen vor allem die Daten der ersten EEG-Messung (t1) ohne Einfluss jeglicher relevanter Medikation, die Daten der zweiten EEG-Messung (Challenge; t2), welche 60 Minuten nach der Einnahme eines der drei zur Verf{\"u}gung stehenden Medikamente (Methylphenidat MPH 20 mg, Atomoxetin ATX 20 mg oder Placebo) erhoben wurden, und die Langzeitergebnisse nach ca. 28 Tagen Behandlungsdauer (t3) mit Methylphenidat (MPH) oder Atomoxetin (ATX) untersucht werden. Zur {\"U}berpr{\"u}fung der Alternativhypothesen H1: μ > μ0, wurden jeweils die Hirnstr{\"o}me der Placebo-Gruppe mit denen der Medikamentengruppen (MTP und ATX) verglichen. Zur {\"U}berpr{\"u}fung der Alternativhypothese H2: µ1 ≠ µ2, wurden die beiden Wirkstoffgruppen (ATX und MTP) miteinander verglichen. Auswertbar waren zum Zeitpunkt der Challenge die Daten von 30 Patienten, zum Zeitpunkt des Follow-Ups noch 28 Patientendaten. Ergebnisse: 1. Es ergab sich ein signifikanter Unterschied der relativen P150-Amplitude unter Therapie mit Methylphenidat zwischen der Baseline (t1) und der Challenge (t2) {\"u}ber Elektrodenposition Fz. 2. Es ergab sich ein signifikanter Unterschied der Amplitude der N2 unter Therapie mit Atomoxetin sowohl zwischen der Baseline- (t1) und der Challenge- (t2) also auch zwischen der Baseline- (t1) und der Behandlungsmessung (t3). Im Rahmen der Challenge-Untersuchung trat ein vergleichbarer Effekt auch in der Placebogruppe auf. Außerdem zeigte die Amplitude der N2 sowohl unter Atomoxetin als auch in der Placebogruppe Anstiege zwischen der Baseline (t1) und der Challenge (t2), welche f{\"u}r die Methylphenidatgruppe nicht beobachtet wurden. Diskussion: Das Potential P150 repr{\"a}sentiert Filterung und gerichteter Aufmerksamkeit. Diese Komponenten werden durch die kurzfristige Einnahme von Methylphenidat beeinflusst. Einen Zusammenhang zwischen Dopaminaktivit{\"a}t im pr{\"a}frontalen Kortex und verbesserter Aufmerksamkeit konnte k{\"u}rzlich gezeigt werden (Rubia et al., 2011). Unsere Ergebnisse k{\"o}nnen diesen Zusammenhang best{\"a}tigen und zeigen zudem eine direkte Korrelation zwischen der Einnahme von Mehtylphenidat und dem Potential P150. Ein Ansprechen der P150 auf Methylphenidat repr{\"a}sentiert somit eine Verbesserung der Aufmerksamkeit. Das Potential N2 repr{\"a}sentiert Inhibition und somit, die Impulsivit{\"a}t. Diese wird sowohl durch die kurzfristige, als auch durch die l{\"a}ngerfristige Einnahme von Atomoxetin beeinflusst. Analog der o. g. Ergebnisse kann somit von einem Effekt des selektiven Noradrenalin Wiederaufnahmehemmer auf die Symptomatik der Impulsivit{\"a}t ausgegangen werden. Eine Korrelation von Atomoxetin und der Aktivit{\"a}t des rechten inferioren, frontalen Kortex konnte ebenfalls bereits gezeigt werden (Chamberlain et al., 2008). Auch diese Ergebnisse k{\"o}nnen wir mit unserer Studie best{\"a}tigen und zudem eine Korrelation zwischen der Einnahme von Atomoxetin und dem Potential N2 aufzeigen. Ein Ansprechen der N2 unter Methylphenidat repr{\"a}sentiert somit eine verbesserte Inhibtionskontrolle und somit eine verminderte Impulsivit{\"a}t. Somit konnte gezeigt werden, dass beide Medikamente auf unterschiedliche Teilsymptome des ADHS wirken.},
  subject      = {P150},
  language  = {de}
}
@phdthesis{Olmes2013,
  author    = {Olmes, David-Gerhard},
  title     = {Beteiligung der adulten Neurogenese bei schizophrenen Psychosen},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-105431},
  school      = {Universit{\"a}t W{\"u}rzburg},
  year      = {2013},
  abstract  = {Hintergrund: Schizophrenie-Spektrumerkrankungen sind h{\"a}ufige, schwerwiegende psychische Erkrankungen, die ein hohes Leid bei Betroffenen und ihren Angeh{\"o}rigen verursachen. Trotz intensiver Bem{\"u}hungen ist die {\"A}tiopathogenese dieser Erkrankungen bislang nur unzureichend verstanden, die Behandlung bislang nur symptomatisch m{\"o}glich, wenngleich eine Wechselwirkung zwischen genetischen und umweltbezogenen Faktoren als urs{\"a}chlich erscheint. Vorherige Arbeiten an frisch gefrorenem Hippokampusgewebe konnten zeigen, dass die adulte Neurogenese in der Subgranularzellschicht des Hippokampus bei an Schizophrenie Erkrankten vermindert ist. Weiterhin gibt es Hinweise f{\"u}r eine Beteiligung des cholinergen Systems und von M1-Acetylcholinrezeptoren bei der Entstehung der psychotischen Symptomatik. Ebenfalls konnte bereits in der Vergangenheit ein Mausmodell generiert werden, das schizophrenieartiges Verhalten zeigt und bei dem der M1-Acetylcholinrezeptor ausgeschaltet ist. Material und Methoden: Im Rahmen der vorliegenden Arbeit wurde zun{\"a}chst eine F{\"a}rbung gegen das Ki-67 Antigen als Marker f{\"u}r proliferative Aktivit{\"a}t in lange Zeit gelagertem Formalin-fixiertem und paraffiniertem Hirngewebe etabliert. Anschließend wurde eine postmortale Fall-Kontroll-Studie in lange Zeit gelagertem, in Formalin fixiertem und paraffiniertem Hippokampusgewebe durchgef{\"u}hrt, bei der die Zahl proliferativ aktiver Zellen, die gegen Ki-67 anf{\"a}rbbar waren, untersucht wurde. Hierbei wurden sowohl gegen Ki-67 anf{\"a}rbbare Zellen in der Subgranularzellschicht, als auch im Hilus ausgewertet. Es standen Hippokampi von 18 schizophren Erkrankten sowie 37 Hippokampi gesunder Kontrollen, die aus zwei verschiedenen Hirnbanken rekrutiert werden mussten, zur Verf{\"u}gung. Die statistische Analyse erfolgte mithilfe eines Kruskal-Wallis Tests sowie bei signifikanten Ergebnissen in diesem mit einem Mann-Whitney U Test. Des Weiteren wurde eine F{\"a}rbung gegen das Ki-67 Antigen in frisch gefrorenen Gehirnen von m{\"a}nnlichen M{\"a}usen durchgef{\"u}hrt; hierbei wurden zw{\"o}lf wildtypische M{\"a}use mit zw{\"o}lf M{\"a}usen mit einer Ausschaltung des M1-Acetylcholinrezeptors vergleichen, wobei letztere schizophrenieartiges Verhalten zeigen. Die Auswertung erfolgte mittels eines zweiseitigen t-Tests. Ergebnisse: Eine F{\"a}rbung gegen Ki-67 in lange Zeit gelagertem, Formalin-fixiertem und in Paraffin eingebettetem Gewebe konnte etabliert werden. Bei Analyse der humanen Fall-Kontroll-Studie konnte ein Trend zu einer verminderten adulten Neurogenese in der hippokampalen Subgranularzone bei schizophrenen Pateinten gefunden werden. Ein signifikanter Unterschied konnte im Vergleich der F{\"a}lle und einer Subgruppe von Kontrollen gefunden werden, die jedoch aus einer anderen Hirnbank als die F{\"a}lle stammten. Keine Signifikanz konnte bei Vergleich der F{\"a}lle mit den Kontrollen aus der gleichen Hirnbank oder bei Vergleich der Ki-67 positiven Zellen in der Hilusregion gefunden werden. Im Mausmodell konnte im Sinne der Hypothese einer verminderten adulten Neurogenese in den M1-Rezeptor knockout-Tieren eine signifikante Reduktion Ki-67 positiver Zellen im Vergleich zu wildtypischen Tieren gezeigt werden, wenn Zellnester anstatt einzelner Zellen gez{\"a}hlt wurden. Diskussion: Es konnte ein Trend hin zu einer verminderten hippokampalen adulten Neurogenese in der Subgranularzellschicht bei an Schizophrenie Erkrankten aufgezeigt werden. Aufgrund der Heterogenit{\"a}t der Proben sind die Ergebnisse jedoch vorsichtig zu bewerten, da Unterschiede in der Vorbehandlung der Proben unter Umst{\"a}nden auch die Ergebnisse erkl{\"a}ren k{\"o}nnten, sodass die Ausgangshypothese einer verminderten hippokampalen adulten Neurogenese nicht sicher widerlegt, aber auch nicht gest{\"u}tzt werden kann; weitere Forschung scheint hier notwendig zu sein. Im Mausmodell konnte eine verminderte hippokampale Neurogenese bei M1-Rezeptor knockout-M{\"a}usen nachgewiesen werden. Dieser Effekt ließ sich nachweisen, wenn große Zellnester betrachtet wurden, was f{\"u}r eine Modulation der Aktivit{\"a}t der neurogenen Niche bei den M1-defizienten Tieren spricht.},
  subject      = {Schizophrenie},
  language  = {de}
}
@article{HarrisMaxwellO'Connoretal.2013,
  author    = {Harris, Fiona M. and Maxwell, Margaret and O'Connor, Rory C. and Coyne, James and Arensman, Ella and Andr{\´a}s, Sz{\´e}kely and Gusm{\~a}o, Ricardo and Coffey, Claire and Costa, Susana and Zoltan, Cserh{\´a}ti and Koburger, Nicole and van Audenhove, Chantal and McDaid, David and Maloney, Julia and V{\"a}rnik, Peeter and Hegerl, Ulrich},
  title     = {Developing social capital in implementing a complex intervention: a process evaluation of the early implementation of a suicide prevention intervention in four European countries},
  series = {BMC Public Health},
  volume    = {13},
  journal   = {BMC Public Health},
  number    = {158},
  doi       = {10.1186/1471-2458-13-158},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122117},
  year      = {2013},
  abstract  = {Background: Variation in the implementation of complex multilevel interventions can impact on their delivery and outcomes. Few suicide prevention interventions, especially multilevel interventions, have included evaluation of both the process of implementation as well as outcomes. Such evaluation is essential for the replication of interventions, for interpreting and understanding outcomes, and for improving implementation science. This paper reports on a process evaluation of the early implementation stage of an optimised suicide prevention programme (OSPI-Europe) implemented in four European countries. Methods: The process analysis was conducted within the framework of a realist evaluation methodology, and involved case studies of the process of implementation in four European countries. Datasets include: repeated questionnaires to track progress of implementation including delivery of individual activities and their intensity; serial interviews and focus groups with stakeholder groups; and detailed observations at OSPI implementation team meetings. Results: Analysis of local contexts in each of the four countries revealed that the advisory group was a key mechanism that had a substantial impact on the ease of implementation of OSPI interventions, particularly on their ability to recruit to training interventions. However, simply recruiting representatives of key organisations into an advisory group is not sufficient to achieve impact on the delivery of interventions. In order to maximise the potential of high level 'gatekeepers', it is necessary to first transform them into OSPI stakeholders. Motivations for OSPI participation as a stakeholder included: personal affinity with the shared goals and target groups within OSPI; the complementary and participatory nature of OSPI that adds value to pre-existing suicide prevention initiatives; and reciprocal reward for participants through access to the extended network capacity that organisations could accrue for themselves and their organisations from participation in OSPI. Conclusions: Exploring the role of advisory groups and the meaning of participation for these participants revealed some key areas for best practice in implementation: careful planning of the composition of the advisory group to access target groups; the importance of establishing common goals; the importance of acknowledging and complementing existing experience and activity; and facilitating an equivalence of benefit from network participation.},
  language  = {en}
}
@article{VernerHerrmannTrocheetal.2013,
  author    = {Verner, Martin and Herrmann, Martin J. and Troche, Stefan J. and Roebers, Claudia M. and Rammsayer, Thomas H.},
  title     = {Cortical oxygen consumption in mental arithmetic as a function of task difficulty: a near-infrared spectroscopy approach},
  series = {Frontiers in Human Neuroscience},
  volume    = {7},
  journal   = {Frontiers in Human Neuroscience},
  number    = {217},
  issn      = {1662-5161},
  doi       = {10.3389/fnhum.2013.00217},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122449},
  year      = {2013},
  abstract  = {The present study investigated changes in cortical oxygenation during mental arithmetic using near-infrared spectroscopy (NIRS). Twenty-nine male volunteers were examined using a 52-channel continuous wave system for analyzing activity in prefrontal areas. With the help of a probabilistic mapping method, three regions of interest (ROIs) on each hemisphere were defined: The inferior frontal gyri (IFG), the middle frontal gyri (MFG), and the superior frontal gyri (SFG). Oxygenation as an indicator of functional brain activation was compared over the three ROI and two levels of arithmetic task difficulty (simple and complex additions). In contrast to most previous studies using fMRI or NIRS, in the present study arithmetic tasks were presented verbally in analogue to many daily life situations. With respect to task difficulty, more complex addition tasks led to higher oxygenation in all defined ROI except in the left IFG compared to simple addition tasks. When compared to the channel positions covering different gyri of the temporal lobe, the observed sensitivity to task complexity was found to be restricted to the specified ROIs. As to the comparison of ROIs, the highest oxygenation was found in the IFG, while MFG and SFG showed significantly less activation compared to IFG. The present cognitive-neuroscience approach demonstrated that NIRS is a suitable and highly feasible research tool for investigating and quantifying neural effects of increasing arithmetic task difficulty.},
  language  = {en}
}
@article{BorchersMuellerSynofziketal.2013,
  author    = {Borchers, Svenja and M{\"u}ller, Laura and Synofzik, Matthis and Himmelbach, Marc},
  title     = {Guidelines and quality measures for the diagnosis of optic ataxia},
  series = {Frontiers in Human Neuroscience},
  volume    = {7},
  journal   = {Frontiers in Human Neuroscience},
  number    = {324},
  issn      = {1662-5161},
  doi       = {10.3389/fnhum.2013.00324},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-122439},
  year      = {2013},
  abstract  = {Since the first description of a systematic mis-reaching by Balint in 1909, a reasonable number of patients showing a similar phenomenology, later termed optic ataxia (OA), has been described. However, there is surprising inconsistency regarding the behavioral measures that are used to detect OA in experimental and clinical reports, if the respective measures are reported at all. A typical screening method that was presumably used by most researchers and clinicians, reaching for a target object in the peripheral visual space, has never been evaluated. We developed a set of instructions and evaluation criteria for the scoring of a semi-standardized version of this reaching task. We tested 36 healthy participants, a group of 52 acute and chronic stroke patients, and 24 patients suffering from cerebellar ataxia. We found a high interrater reliability and a moderate test-retest reliability comparable to other clinical instruments in the stroke sample. The calculation of cut-off thresholds based on healthy control and cerebellar patient data showed an unexpected high number of false positives in these samples due to individual outliers that made a considerable number of errors in peripheral reaching. This study provides first empirical data from large control and patient groups for a screening procedure that seems to be widely used but rarely explicitly reported and prepares the grounds for its use as a standard tool for the description of patients who are included in single case or group studies addressing optic ataxia similar to the use of neglect, extinction, or apraxia screening tools.},
  language  = {en}
}
@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{BonnSchmittLeschetal.2013,
  author    = {Bonn, M. and Schmitt, A. and Lesch, K.-P. and Van Bockstaele, E. J. and Asan, E.},
  title     = {Serotonergic innervation and serotonin receptor expression of NPY-producing neurons in the rat lateral and basolateral amygdaloid nuclei},
  series = {Brain Structure and Function},
  volume    = {218},
  journal   = {Brain Structure and Function},
  number    = {2},
  doi       = {10.1007/s00429-012-0406-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132591},
  pages     = {421-435},
  year      = {2013},
  abstract  = {Pharmacobehavioral studies in experimental animals, and imaging studies in humans, indicate that serotonergic transmission in the amygdala plays a key role in emotional processing, especially for anxiety-related stimuli. The lateral and basolateral amygdaloid nuclei receive a dense serotonergic innervation in all species studied to date. We investigated interrelations between serotonergic afferents and neuropeptide Y (NPY)-producing neurons, which are a subpopulation of inhibitory interneurons in the rat lateral and basolateral nuclei with particularly strong anxiolytic properties. Dual light microscopic immunolabeling showed numerous appositions of serotonergic afferents on NPY-immunoreactive somata. Using electron microscopy, direct membrane appositions and synaptic contacts between serotonin-containing axon terminals and NPY-immunoreactive cellular profiles were unequivocally established. Double in situ hybridization documented that more than 50 \%, and about 30-40 \% of NPY mRNA-producing neurons, co-expressed inhibitory 5-HT1A and excitatory 5-HT2C mRNA receptor subtype mRNA, respectively, in both nuclei with no gender differences. Triple in situ hybridization showed that individual NPY mRNA-producing interneurons co-express both 5-HT1A and 5-HT2C mRNAs. Co-expression of NPY and 5-HT3 mRNA was not observed. The results demonstrate that serotonergic afferents provide substantial innervation of NPY-producing neurons in the rat lateral and basolateral amygdaloid nuclei. Studies of serotonin receptor subtype co-expression indicate a differential impact of the serotonergic innervation on this small, but important, population of anxiolytic interneurons, and provide the basis for future studies of the circuitry underlying serotonergic modulation of emotional stimulus processing in the amygdala.},
  language  = {en}
}
@article{HornSchellerduPlessisetal.2013,
  author    = {Horn, Anne and Scheller, Carsten and du Plessis, Stefan and Arendt, Gabriele and Nolting, Thorsten and Joska, John and Sopper, Sieghart and Maschke, Matthias and Obermann, Mark and Husstedt, Ingo W. and Hain, Johannes and Maponga, Tongai and Riederer, Peter and Koutsilieri, Eleni},
  title     = {Increases in CSF dopamine in HIV patients are due to the dopamine transporter 10/10-repeat allele which is more frequent in HIV-infected individuals},
  series = {Journal of Neural Transmission},
  volume    = {120},
  journal   = {Journal of Neural Transmission},
  doi       = {10.1007/s00702-013-1086-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-132385},
  pages     = {1411-1419},
  year      = {2013},
  abstract  = {Dysfunction of dopaminergic neurotransmission has been implicated in HIV infection. We showed previously increased dopamine (DA) levels in CSF of therapy-na{\"i}ve HIV patients and an inverse correlation between CSF DA and CD4 counts in the periphery, suggesting adverse effects of high levels of DA on HIV infection. In the current study including a total of 167 HIV-positive and negative donors from Germany and South Africa (SA), we investigated the mechanistic background for the increase of CSF DA in HIV individuals. Interestingly, we found that the DAT 10/10-repeat allele is present more frequently within HIV individuals than in uninfected subjects. Logistic regression analysis adjusted for gender and ethnicity showed an odds ratio for HIV infection in DAT 10/10 allele carriers of 3.93 (95 \% CI 1.72-8.96; p = 0.001, Fishers exact test). 42.6 \% HIV-infected patients harbored the DAT 10/10 allele compared to only 10.5 \% uninfected DAT 10/10 carriers in SA (odds ratio 6.31), whereas 68.1 versus 40.9 \%, respectively, in Germany (odds ratio 3.08). Subjects homozygous for the 10-repeat allele had higher amounts of CSF DA and reduced DAT mRNA expression but similar disease severity compared with those carrying other DAT genotypes. These intriguing and novel findings show the mutual interaction between DA and HIV, suggesting caution in the interpretation of CNS DA alterations in HIV infection solely as a secondary phenomenon to the virus and open the door for larger studies investigating consequences of the DAT functional polymorphism on HIV epidemiology and progression of disease.},
  language  = {en}
}
@article{PfeifferGoetzXiangetal.2013,
  author    = {Pfeiffer, Verena and G{\"o}tz, Rudolf and Xiang, Chaomei and Camarero, Guadelupe and Braun, Attila and Zhang, Yina and Blum, Robert and Heinsen, Helmut and Nieswandt, Bernhard and Rapp, Ulf R.},
  title     = {Ablation of BRaf Impairs Neuronal Differentiation in the Postnatal Hippocampus and Cerebellum},
  series = {PLoS ONE},
  volume    = {8},
  journal   = {PLoS ONE},
  number    = {3},
  doi       = {10.1371/journal.pone.0058259},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130304},
  pages     = {e58259},
  year      = {2013},
  abstract  = {This study focuses on the role of the kinase BRaf in postnatal brain development. Mice expressing truncated, non-functional BRaf in neural stem cell-derived brain tissue demonstrate alterations in the cerebellum, with decreased sizes and fuzzy borders of the glomeruli in the granule cell layer. In addition we observed reduced numbers and misplaced ectopic Purkinje cells that showed an altered structure of their dendritic arborizations in the hippocampus, while the overall cornus ammonis architecture appeared to be unchanged. In male mice lacking BRaf in the hippocampus the size of the granule cell layer was normal at postnatal day 12 (P12) but diminished at P21, as compared to control littermates. This defect was caused by a reduced ability of dentate gyrus progenitor cells to differentiate into NeuN positive granule cell neurons. In vitro cell culture of P0/P1 hippocampal cells revealed that BRaf deficient cells were impaired in their ability to form microtubule-associated protein 2 positive neurons. Together with the alterations in behaviour, such as autoaggression and loss of balance fitness, these observations indicate that in the absence of BRaf all neuronal cellular structures develop, but neuronal circuits in the cerebellum and hippocampus are partially disturbed besides impaired neuronal generation in both structures.},
  language  = {en}
}
@article{HohoffGorjiKaiseretal.2013,
  author    = {Hohoff, Christa and Gorji, Ali and Kaiser, Sylvia and Willscher, Edith and Korsching, Eberhard and Ambr{\´e}e, Oliver and Arolt, Volker and Lesch, Klaus-Peter and Sachser, Norbert and Deckert, J{\"u}rgen and Lewejohann, Lars},
  title     = {Effect of Acute Stressor and Serotonin Transporter Genotype on Amygdala First Wave Transcriptome in Mice},
  series = {PLoS ONE},
  volume    = {8},
  journal   = {PLoS ONE},
  number    = {3},
  doi       = {10.1371/journal.pone.0058880},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-131040},
  pages     = {e58880},
  year      = {2013},
  abstract  = {The most prominent brain region evaluating the significance of external stimuli immediately after their onset is the amygdala. Stimuli evaluated as being stressful actuate a number of physiological processes as an immediate stress response. Variation in the serotonin transporter gene has been associated with increased anxiety- and depression-like behavior, altered stress reactivity and adaptation, and pathophysiology of stress-related disorders. In this study the instant reactions to an acute stressor were measured in a serotonin transporter knockout mouse model. Mice lacking the serotonin transporter were verified to be more anxious than their wild-type conspecifics. Genome-wide gene expression changes in the amygdala were measured after the mice were subjected to control condition or to an acute stressor of one minute exposure to water. The dissection of amygdalae and stabilization of RNA was conducted within nine minutes after the onset of the stressor. This extremely short protocol allowed for analysis of first wave primary response genes, typically induced within five to ten minutes of stimulation, and was performed using Affymetrix GeneChip Mouse Gene 1.0 ST Arrays. RNA profiling revealed a largely new set of differentially expressed primary response genes between the conditions acute stress and control that differed distinctly between wild-type and knockout mice. Consequently, functional categorization and pathway analysis indicated genes related to neuroplasticity and adaptation in wild-types whereas knockouts were characterized by impaired plasticity and genes more related to chronic stress and pathophysiology. Our study therefore disclosed different coping styles dependent on serotonin transporter genotype even directly after the onset of stress and accentuates the role of the serotonergic system in processing stressors and threat in the amygdala. Moreover, several of the first wave primary response genes that we found might provide promising targets for future therapeutic interventions of stress-related disorders also in humans.},
  language  = {en}
}