@article{Conzelmann2012, abstract = {RATIONALE: The endocannabinoid (eCB) system is implicated in several psychiatric disorders. Investigating emotional-motivational dysfunctions as underlying mechanisms, a study in humans revealed that in the C385A polymorphism of the fatty acid amide hydrolase (FAAH), the degrading enzyme of the eCB anandamide (AEA), A carriers, who are characterized by increased signaling of AEA as compared to C/C carriers, exhibited reduced brain reactivity towards unpleasant faces and enhanced reactivity towards reward. However, the association of eCB system with emotional-motivational reactivity is complex and bidirectional due to upcoming compensatory processes. OBJECTIVES: Therefore, we further investigated the relationship of the FAAH polymorphism and emotional-motivational reactivity in humans. METHODS: We assessed the affect-modulated startle, and ratings of valence and arousal in response to higher arousing pleasant, neutral, and unpleasant pictures in 67 FAAH C385A C/C carriers and 45 A carriers. RESULTS: Contrarily to the previous functional MRI study, A carriers compared to C/C carriers exhibited an increased startle potentiation and therefore emotional responsiveness towards unpleasant picture stimuli and reduced startle inhibition indicating reduced emotional reactivity in response to pleasant pictures, while both groups did not differ in ratings of arousal and valence. CONCLUSIONS: Our findings emphasize the bidirectionality and thorough examination of the eCB system's impact on emotional reactivity as a central endophenotype underlying various psychiatric disorders.}, author = {Conzelmann, Annette and Reif, Andreas and Jacob, Christian and Weyers, Peter and Lesch, Klaus-Peter and Lutz, Beat and Pauli, Paul}, doi = {10.1007/s00213-012-2785-y}, journal = {Psychopharmacology}, month = {jul}, pages = {573-579}, title = {A polymorphism in the gene of the endocannabinoid-degrading enzyme FAAH (FAAH C385A) is associated with emotional–motivational reactivity}, url = {https://link.springer.com/content/pdf/10.1007%2Fs00213-012-2785-y.pdf}, volume = {224}, year = {2012} } @misc{Conzelmann2012_2, author = {Conzelmann, Annette and Reif, Andreas and Jacob, Christian and Weyers, Peter and Lesch, Klaus-Peter and Lutz, Beat and Pauli, Paul}, month = {jul}, title = {Supplementary Material}, year = {2012} } @article{Dentel2012, abstract = {Spasticity is a common and disabling symptom observed in patients with central nervous system diseases, including amyotrophic lateral sclerosis, a disease affecting both upper and lower motor neurons. In amyotrophic lateral sclerosis, spasticity is traditionally thought to be the result of degeneration of the upper motor neurons in the cerebral cortex, although degeneration of other neuronal types, in particular serotonergic neurons, might also represent a cause of spasticity. We performed a pathology study in seven patients with amyotrophic lateral sclerosis and six control subjects and observed that central serotonergic neurons suffer from a degenerative process with prominent neuritic degeneration, and sometimes loss of cell bodies in patients with amyotrophic lateral sclerosis. Moreover, distal serotonergic projections to spinal cord motor neurons and hippocampus systematically degenerated in patients with amyotrophic lateral sclerosis. In SOD1 (G86R) mice, a transgenic model of amyotrophic lateral sclerosis, serotonin levels were decreased in brainstem and spinal cord before onset of motor symptoms. Furthermore, there was noticeable atrophy of serotonin neuronal cell bodies along with neuritic degeneration at disease onset. We hypothesized that degeneration of serotonergic neurons could underlie spasticity in amyotrophic lateral sclerosis and investigated this hypothesis in vivo using tail muscle spastic-like contractions in response to mechanical stimulation as a measure of spasticity. In SOD1 (G86R) mice, tail muscle spastic-like contractions were observed at end-stage. Importantly, they were abolished by 5-hydroxytryptamine-2b/c receptors inverse agonists. In line with this, 5-hydroxytryptamine-2b receptor expression was strongly increased at disease onset. In all, we show that serotonergic neurons degenerate during amyotrophic lateral sclerosis, and that this might underlie spasticity in mice. Further research is needed to determine whether inverse agonists of 5-hydroxytryptamine-2b/c receptors could be of interest in treating spasticity in patients with amyotrophic lateral sclerosis.}, author = {Dentel, Christel and de Aguilar, Jose-Luis Gonzalez and Palamiuc, Lavinia and Henriques, Alexandre and Lannes, Béatrice and Spreux-Varoquaux, Odile and Gutknecht, Lise and René, Frédérique and Echaniz-Laguna, Andoni and Gonzalez de Aguilar, J.-L. and Lesch, Klaus Peter and Meininger, Vincent and Loeffler, Jean-Philippe and Dupuis, Luc}, doi = {10.1093/brain/aws274}, journal = {Brain}, month = {oct}, pages = {483-493}, title = {Degeneration of serotonergic neurons in amyotrophic lateral sclerosis: A link to spasticity}, url = {http://doi.org/10.1093/brain/aws274}, volume = {136}, year = {2012} } @article{Enge2012, author = {Enge, Sören and Fleischhauer, Monika and Lesch, Klaus-Peter and Reif, Andreas and Strobel, Alexander}, doi = {10.1093/cercor/bhs398}, journal = {Cerebral Cortex}, month = {dec}, pages = {1195-1205}, title = {Variation in Key Genes of Serotonin and Norepinephrine Function Predicts Gamma-Band Activity during Goal-Directed Attention}, url = {https://academic.oup.com/cercor/article-pdf/24/5/1195/14101017/bhs398.pdf}, volume = {24}, year = {2012} } @article{Fallgatter2012, abstract = {Current research strategies have made great efforts to further elucidate the complex genetic architecture of attention-deficit hyperactivity disorder (ADHD). The present study examined the impact of an LPHN3 haplotype that has recently been associated with ADHD (Arcos-Burgos et al., 2010) on neural activity in a visual Go-NoGo task. Two hundred sixteen adult ADHD patients completed a Continuous Performance Test (CPT) while the ongoing EEG was simultaneously recorded. Results showed that patients carrying two copies of the LPHN3 risk haplotype (n=114) made more omission errors and had a more anterior Go-centroid of the P300 than patients carrying at least one LPHN3 non-risk haplotype (n=102). Accordingly, the NoGo-Anteriorization (NGA; topographical ERP difference of the Go- and NoGo-condition), a neurophysiological marker of prefrontal functioning, was reduced in the LPHN3 high risk group. However, in the NoGo-condition itself no marked differences attributable to the LPHN3 haplotype could be found. Our findings indicate that, within a sample of ADHD patients, the LPHN3 gene impacts behavioral and neurophysiological measures of cognitive response control. The results of our study further strengthen the concept of an LPHN3 risk haplotype for ADHD and support the usefulness of the endophenotype approach in psychiatric and psychological research.}, author = {Fallgatter, Andreas J. and Ehlis, Ann-Christine and Dresler, Thomas and Reif, Andreas and Jacob, Christian P. and Arcos-Burgos, Mauricio and Muenke, Maximilian and Lesch, Klaus-Peter}, doi = {10.1016/j.euroneuro.2012.11.001}, journal = {European Neuropsychopharmacology}, month = {dec}, pages = {458-468}, title = {Influence of a Latrophilin 3 (LPHN3) risk haplotype on event-related potential measures of cognitive response control in attention-deficit hyperactivity disorder (ADHD)}, url = {http://www.ncbi.nlm.nih.gov/pubmed/23245769}, volume = {23}, year = {2012} } @article{Gutknecht2012, abstract = {Brain serotonin (5-HT) is implicated in a wide range of functions from basic physiological mechanisms to complex behaviors, including neuropsychiatric conditions, as well as in developmental processes. Increasing evidence links 5-HT signaling alterations during development to emotional dysregulation and psychopathology in adult age. To further analyze the importance of brain 5-HT in somatic and brain development and function, and more specifically differentiation and specification of the serotonergic system itself, we generated a mouse model with brain-specific 5-HT deficiency resulting from a genetically driven constitutive inactivation of neuronal tryptophan hydroxylase-2 (Tph2). Tph2 inactivation (Tph2-/-) resulted in brain 5-HT deficiency leading to growth retardation and persistent leanness, whereas a sex- and age-dependent increase in body weight was observed in Tph2+/- mice. The conserved expression pattern of the 5-HT neuron-specific markers (except Tph2 and 5-HT) demonstrates that brain 5-HT synthesis is not a prerequisite for the proliferation, differentiation and survival of raphe neurons subjected to the developmental program of serotonergic specification. Furthermore, although these neurons are unable to synthesize 5-HT from the precursor tryptophan, they still display electrophysiological properties characteristic of 5-HT neurons. Moreover, 5-HT deficiency induces an up-regulation of 5-HT\(_{1A}\) and 5-HT\(_{1B}\) receptors across brain regions as well as a reduction of norepinephrine concentrations accompanied by a reduced number of noradrenergic neurons. Together, our results characterize developmental, neurochemical, neurobiological and electrophysiological consequences of brain-specific 5-HT deficiency, reveal a dual dose-dependent role of 5-HT in body weight regulation and show that differentiation of serotonergic neuron phenotype is independent from endogenous 5-HT synthesis.}, author = {Gutknecht, Lise and Araragi, Naozumi and Merker, Sören and Waider, Jonas and Sommerlandt, Frank M. J. and Mlinar, Boris and Baccini, Gilda and Mayer, Ute and Proft, Florian and Hamon, Michel and Schmitt, Angelika G. and Corradetti, Renato and Lanfumey, Laurence and Lesch, Klaus-Peter}, doi = {10.1371/journal.pone.0043157}, journal = {PLoS ONE}, month = {aug}, pages = {e43157}, title = {Impacts of Brain Serotonin Deficiency following Tph2 Inactivation on Development and Raphe Neuron Serotonergic Specification}, url = {http://dx.doi.org/10.1371/journal.pone.0043157}, volume = {7}, year = {2012} } @misc{Gutknecht2012_2, author = {Gutknecht, Lise and Araragi, Naozumi and Merker, Sören and Waider, Jonas and Sommerlandt, Frank M. J. and Mlinar, Boris and Baccini, Gilda and Mayer, Ute and Proft, Florian and Hamon, Michel and Schmitt, Angelika G. and Corradetti, Renato and Lanfumey, Laurence and Lesch, Klaus-Peter}, month = {aug}, title = {Table S1}, year = {2012} } @article{Heinzel2012, author = {Heinzel, Sebastian and Baehne, Christina G. and Dresler, Thomas and Jacob, Christian P. and Heine, Monika and Renner, Tobias J. and Boreatti-Hümmer, Andrea and Reif, Andreas and Lesch, Klaus-Peter and Fallgatter, Andreas J. and Ehlis, Ann-Christine}, doi = {10.1093/cercor/bhs132}, journal = {Cerebral Cortex}, month = {may}, pages = {1453-1462}, title = {COMT x DRD4 Epistasis Impacts Prefrontal Cortex Function Underlying Response Control}, url = {https://academic.oup.com/cercor/article-pdf/23/6/1453/17307876/bhs132.pdf}, volume = {23}, year = {2012} } @article{Hinney2012, author = {Hinney, Anke and Scherag, André and Jarick, Ivonne and Albayrak, Özgür and Pütter, Carolin and Pechlivanis, Sonali and Dauvermann, Maria R. and Beck, Sebastian and Weber, Heike and Scherag, Susann and Nguyen, Trang T. and Volckmar, Anna-Lena and Knoll, Nadja and Faraone, Stephen V. and Neale, Benjamin M. and Franke, Barbara and Cichon, Sven and Hoffmann, Per and Nöthen, Markus M. and Schreiber, Stefan and Jöckel, Karl-Heinz and Wichmann, H.-Erich and Freitag, Christine and Lempp, Thomas and Meyer, Jobst and Gilsbach, Susanne and Herpertz-Dahlmann, Beate and Sinzig, Judith and Lehmkuhl, Gerd and Renner, Tobias J. and Warnke, Andreas and Romanos, Marcel and Lesch, Klaus-Peter and Reif, Andreas and Schimmelmann, Benno G. and Hebebrand, Johannes}, doi = {10.1002/ajmg.b.32056}, journal = {American Journal of Medical Genetics Part B: Neuropsychiatric Genetics}, month = {may}, pages = {476-476}, title = {Addendum: Genome-wide association study in German patients with attention deficit/hyperactivity disorder}, url = {http://onlinelibrary.wiley.com/doi/10.1002/ajmg.b.32056/pdf}, volume = {159B}, year = {2012} } @article{Ineichen2012, abstract = {Valid animal models of psychopathology need to include behavioural readouts informed by human findings. In the probabilistic reversal learning (PRL) task, human subjects are confronted with serial reversal of the contingency between two operant stimuli and reward/punishment and, superimposed on this, a low probability (0.2) of punished correct responses/rewarded incorrect responses. In depression, reward-stay and reversals completed are unaffected but response-shift following punished correct response trials, referred to as negative feedback sensitivity (NFS), is increased. The aims of this study were to: establish an operant spatial PRL test appropriate for mice; obtain evidence for the processes mediating reward-stay and punishment-shift responding; and assess effects thereon of genetically- and pharmacologically-altered serotonin (5-HT) function. The study was conducted with wildtype (WT) and heterozygous mutant (HET) mice from a 5-HT transporter (5-HTT) null mutant strain. Mice were mildly food deprived and reward was sugar pellet and punishment was 5-s time out. Mice exhibited high motivation and adaptive reversal performance. Increased probability of punished correct response (PCR) trials per session (p = 0.1, 0.2 or 0.3) led to monotonic decrease in reward-stay and reversals completed, suggesting accurate reward prediction. NFS differed from chance-level at p PCR = 0.1, suggesting accurate punishment prediction, whereas NFS was at chance-level at p = 0.2-0.3. At p PCR = 0.1, HET mice exhibited lower NFS than WT mice. The 5-HTT blocker escitalopram was studied acutely at p PCR = 0.2: a low dose (0.5-1.5 mg/kg) resulted in decreased NFS, increased reward-stay and increased reversals completed, and similarly in WT and HET mice. This study demonstrates that testing PRL in mice can provide evidence on the regulation of reward and punishment processing that is, albeit within certain limits, of relevance to human emotional-cognitive processing, its dysfunction and treatment.}, author = {Ineichen, Christian and Sigrist, Hannes and Spinelli, Simona and Lesch, Klaus-Peter and Sautter, Eva and Seifritz, Erich and Pryce, Christopher R.}, doi = {10.1016/j.neuropharm.2012.07.025}, journal = {Neuropharmacology}, month = {jul}, pages = {1012-1021}, title = {Establishing a probabilistic reversal learning test in mice: Evidence for the processes mediating reward-stay and punishment-shift behaviour and for their modulation by serotonin}, url = {https://www.researchgate.net/profile/Christian_Ineichen/publication/229551979_Establishing_a_probabilistic_reversal_learning_test_in_mice_Evidence_for_the_processes_mediating_reward-stay_and_punishment-shift_behaviour_and_for_their_modulation_by_serotonin/links/542964b00cf238c6ea7e2fbb.pdf}, volume = {63}, year = {2012} } @article{Jacob2012, abstract = {There are several lines of evidence that the 4p16 region is a candidate locus of both attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder. None of the harbored candidate genes of this region were hitherto shown to be associated with ADHD despite promising functionality. One of the most promising candidate genes in this region is protein phosphatase 2, regulatory subunit B, gamma (PPP2R2C), which, however, thus far has not been assessed for a potential association with ADHD. A total of 513 in- and outpatients affected with adult ADHD and 536 controls as well as 170 nuclear families with 249 children affected with ADHD were genotyped for 35 SNPs, which tagged the promoter region, the 5' and 3' UTRs, and the exons of the PPP2R2C. Two independent samples provided evidence that the major G allele of rs16838844 increases risk toward ADHD. Allelic variations of PPP2R2C rs16838698 on the other hand might be associated with a variety of personality traits. There is evidence that allelic variation in PPP2R2C may be associated with a variety of personality traits and ADHD per se. Nevertheless, as all those conditions are comorbid, PPP2R2C might reflect a common underlying neurobiological risk factor.}, author = {Jacob, Christian and Nguyen, Thuy Tran and Weißflog, Lena and Herrmann, Martin and Liedel, Stefanie and Zamzow, Karin and Jans, Thomas and Renner, Tobias and Reichert, Susanne and Groß-Lesch, Silke and Lesch, Klaus-Peter and Reif, Andreas}, doi = {10.1007/s12402-012-0080-8}, journal = {ADHD Attention Deficit and Hyperactivity Disorders}, month = {jun}, pages = {145-152}, title = {PPP2R2C as a candidate gene of a temperament and character trait-based endophenotype of ADHD}, url = {https://www.researchgate.net/profile/Andreas_Reif/publication/225185940_PPP2R2C_as_a_candidate_gene_of_a_temperament_and_character_trait-based_endophenotype_of_ADHD/links/0c96052fbeeda5eff1000000.pdf}, volume = {4}, year = {2012} } @article{Jarick2012, abstract = {Attention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable neurodevelopmental disorder. Genetic loci have not yet been identified by genome-wide association studies. Rare copy number variations (CNVs), such as chromosomal deletions or duplications, have been implicated in ADHD and other neurodevelopmental disorders. To identify rare (frequency ⩽1%) CNVs that increase the risk of ADHD, we performed a whole-genome CNV analysis based on 489 young ADHD patients and 1285 adult population-based controls and identified one significantly associated CNV region. In tests for a global burden of large (>500 kb) rare CNVs, we observed a nonsignificant (P=0.271) 1.126-fold enriched rate of subjects carrying at least one such CNV in the group of ADHD cases. Locus-specific tests of association were used to assess if there were more rare CNVs in cases compared with controls. Detected CNVs, which were significantly enriched in the ADHD group, were validated by quantitative (q)PCR. Findings were replicated in an independent sample of 386 young patients with ADHD and 781 young population-based healthy controls. We identified rare CNVs within the parkinson protein 2 gene (PARK2) with a significantly higher prevalence in ADHD patients than in controls (P=2.8 × 10−4 after empirical correction for genome-wide testing). In total, the PARK2 locus (chr 6: 162 659 756–162 767 019) harboured three deletions and nine duplications in the ADHD patients and two deletions and two duplications in the controls. By qPCR analysis, we validated 11 of the 12 CNVs in ADHD patients (P=1.2 × 10−3 after empirical correction for genome-wide testing). In the replication sample, CNVs at the PARK2 locus were found in four additional ADHD patients and one additional control (P=4.3 × 10−2). Our results suggest that copy number variants at the PARK2 locus contribute to the genetic susceptibility of ADHD. Mutations and CNVs in PARK2 are known to be associated with Parkinson disease.}, author = {Jarick, Ivonne and Volckmar, Anna-Lena and Pütter, Carolin and Nguyen, Trang T. and Pechlivanis, Sonali and Beck, Sebastian and Dauvermann, Maria R. and Albayrak, Özgür and Cichon, Sven and Gilsbach, Susanne and Scherag, Susann and Degenhardt, Franziska A. and Hoffmann, Per and Nöthen, Markus M. and Schreiber, Stefan and Wichmann, H.-Erich and Heinrich, Joachim and Jöckel, Karl-Heinz and Faraone, Stephen V. and Tiesler, Carla M. T. and Walitza, Susanne and Sinzig, Judith and Freitag, Christine and Herpertz-Dahlmann, Beate and Meyer, Jobst and Lehmkuhl, Gerd and Renner, Tobias J. and Warnke, Andreas and Lesch, Klaus-Peter and Romanos, Marcel and Reif, Andreas and Hebebrand, Johannes and Schimmelmann, Benno G. and Hinney, Anke and Scherag, André}, doi = {10.1038/mp.2012.161}, journal = {Molecular Psychiatry}, month = {nov}, pages = {115-121}, title = {Genome-wide analysis of rare copy number variations reveals PARK2 as a candidate gene for attention-deficit/hyperactivity disorder}, url = {http://doi.org/10.1038/mp.2012.161}, volume = {19}, year = {2012} } @article{Kurrikoff2012, abstract = {AbstractA functional promoter polymorphism of the nitric oxide synthase 1 gene first exon 1f variable number tandem repeat (NOS1 ex1f-VNTR) is associated with impulsivity and related psychopathology. Facets of impulsivity are strongly associated with personality traits; maladaptive impulsivity with neuroticism; and adaptive impulsivity with extraversion. Both high neuroticism and low extraversion predict anxiety and depressive symptoms. The aim of the present study was to evaluate the effect of the NOS1 ex1f-VNTR genotype and possible interaction with environmental factors on personality, anxiety, and depressiveness in a population-representative sample. Short allele carriers had higher neuroticism and anxiety than individuals with the long/long (l/l) genotype. Male short/short homozygotes also had higher extraversion. In the face of environmental adversity, females with a short allele had higher scores of neuroticism, anxiety, and depressiveness compared to the l/l genotype. Males were more sensitive to environmental conditions when they had the l/l genotype and low extraversion. In conclusion, the NOS1 ex1f-VNTR influences personality and emotional regulation dependent on gender and environment. Together with previous findings on the effect of the NOS1 genotype on impulse control, these data suggest that NOS1 should be considered another plasticity gene, because its variants are associated with different coping strategies.}, author = {Kurrikoff, Triin and Lesch, Klaus-Peter and Kiive, Evelyn and Konstabel, Kenn and Herterich, Sabine and Veidebaum, Toomas and Reif, Andreas and Harro, Jaanus}, doi = {10.1017/s0954579412000661}, journal = {Development and Psychopathology}, month = {oct}, pages = {1225-1235}, title = {Association of a functional variant of the nitric oxide synthase 1 gene with personality, anxiety, and depressiveness}, url = {https://oadoi.org/10.1017/s0954579412000661}, volume = {24}, year = {2012} } @article{Lesch2012, abstract = { Aggression, which comprises multi-faceted traits ranging from negative emotionality to antisocial behaviour, is influenced by an interaction of biological, psychological and social variables. Failure in social adjustment, aggressiveness and violence represent the most detrimental long-term outcome of neurodevelopmental disorders. With the exception of brain-specific tryptophan hydroxylase-2 ( Tph2 ), which generates serotonin (5-HT) in raphe neurons, the contribution of gene variation to aggression-related behaviour in genetically modified mouse models has been previously appraised (Lesch 2005 Novartis Found Symp . 268 , 111–140; Lesch & Merschdorf 2000 Behav. Sci. Law 18 , 581–604). Genetic inactivation of Tph2 function in mice led to the identification of phenotypic changes, ranging from growth retardation and late-onset obesity, to enhanced conditioned fear response, increased aggression and depression-like behaviour. This spectrum of consequences, which are amplified by stress-related epigenetic interactions, are attributable to deficient brain 5-HT synthesis during development and adulthood. Human data relating altered TPH2 function to personality traits of negative emotionality and neurodevelopmental disorders characterized by deficits in cognitive control and emotion regulation are based on genetic association and are therefore not as robust as the experimental mouse results. Mouse models in conjunction with approaches focusing on TPH2 variants in humans provide unexpected views of 5-HT's role in brain development and in disorders related to negative emotionality, aggression and antisocial behaviour. }, author = {Lesch, Klaus-Peter and Araragi, Naozumi and Waider, Jonas and van den Hove, Daniel and Gutknecht, Lise}, doi = {10.1098/rstb.2012.0039}, journal = {Philosophical Transactions of the Royal Society B: Biological Sciences}, month = {sep}, pages = {2426-2443}, title = {Targeting brain serotonin synthesis: insights into neurodevelopmental disorders with long-term outcomes related to negative emotionality, aggression and antisocial behaviour}, url = {http://rstb.royalsocietypublishing.org/content/royptb/367/1601/2426.full.pdf}, volume = {367}, year = {2012} } @article{Lesch2012_2, abstract = {Serotonin (5-HT) shapes brain networks during development and modulates a wide spectrum of essential neuronal functions ranging from perception and cognitive appraisal to emotional responses in the mature brain. Deficits in 5-HT-moderated synaptic signaling fundamentally impact the pathophysiology and long-term outcome of neurodevelopmental disorders. Our understanding of how 5-HT-dependent modulation of circuit configuration influences social cognition and emotional learning has been enhanced by recent insight into the molecular and cellular mechanisms of synapse formation and plasticity. In this review, we discuss emerging concepts as to how defects in synaptic plasticity impact our biosocial brain and how recent findings regarding 5-HT's role in brain development and function provide insight into the cellular and physiological basis of neurodevelopmental disorders.}, author = {Lesch, Klaus-Peter and Waider, Jonas}, doi = {10.1016/j.neuron.2012.09.013}, journal = {Neuron}, month = {oct}, pages = {175-191}, title = {Serotonin in the Modulation of Neural Plasticity and Networks: Implications for Neurodevelopmental Disorders}, url = {https://oadoi.org/10.1016/j.neuron.2012.09.013}, volume = {76}, year = {2012} } @article{Mueller2012, author = {Mueller, Anett and Strahler, Jana and Armbruster, Diana and Lesch, Klaus-Peter and Brocke, Burkhard and Kirschbaum, Clemens}, doi = {10.1016/j.ijpsycho.2011.11.007}, journal = {International Journal of Psychophysiology}, month = {mar}, pages = {302-308}, title = {Genetic contributions to acute autonomic stress responsiveness in children}, url = {https://oadoi.org/10.1016/j.ijpsycho.2011.11.007}, volume = {83}, year = {2012} } @article{RibaséS2012, author = {RibaséS, Marta and Ramos-Quiroga, Josep Antoni and HerváS, Amaia and Sánchez-Mora, Cristina and Bosch, Rosa and Bielsa, Anna and Gastaminza, Xavier and Lesch, Klaus-Peter and Reif, Andreas and Renner, Tobias J. and Romanos, Marcel and Warnke, Andreas and Walitza, Susanne and Freitag, Christine and Meyer, Jobst and Palmason, Haukur and Casas, Miquel and Bayés, Mònica and Cormand, Bru}, doi = {10.3109/15622975.2011.584905}, journal = {The World Journal of Biological Psychiatry}, month = {mar}, pages = {281-292}, title = {Candidate system analysis in ADHD: Evaluation of nine genes involved in dopaminergic neurotransmission identifies association withDRD1}, url = {https://oadoi.org/10.3109/15622975.2011.584905}, volume = {13}, year = {2012} } @article{Ribasés2012, author = {Ribasés, Marta and Sánchez-Mora, Cristina and Ramos-Quiroga, Josep Antoni and Bosch, Rosa and Gómez, Núria and Nogueira, Mariana and Corrales, Montse and Palomar, Gloria and Jacob, Christian P. and Gross-Lesch, Silke and Kreiker, Susanne and Reif, Andreas and Lesch, Klaus Peter and Cormand, Bru and Casas, Miquel and Bayés, Mónica}, doi = {10.1097/ypg.0b013e328353957e}, journal = {Psychiatric Genetics}, month = {apr}, pages = {155-160}, title = {An association study of sequence variants in the forkhead box P2 (FOXP2) gene and adulthood attention-deficit/hyperactivity disorder in two European samples}, url = {https://www.researchgate.net/profile/Bru_Cormand/publication/224038250_An_association_study_of_sequence_variants_in_the_forkhead_box_P2_FOXP2_gene_and_adulthood_attention-deficithyperactivity_disorder_in_two_European_samples/links/00b4952d7a4fac93a1000000.pdf}, volume = {22}, year = {2012} } @article{Sachser2013, abstract = {Zusammenfassung Individuelle Unterschiede im Furcht- und Angstniveau entwickeln sich bei Mensch und Tier im Laufe der Lebensgeschichte, wobei sowohl genetische als auch Umweltfaktoren an der spezifischen Ausprägung dieser Emotionen beteiligt sind. Bezüglich der Umwelt können belastende Lebensereignisse während der Schwangerschaft der Mutter, wie auch negative Erfahrungen während der Kindheit zu verstärkter Ängstlichkeit im späteren Leben führen. Aus klinischer Sicht ist die Wahrscheinlichkeit für die Entwicklung von Angsterkrankungen dann erhöht. Interessanterweise behalten die Angstschaltkreise im Zentralnervensystem ihre Plastizität bis ins Erwachsenenalter. Entsprechend ist das Angstniveau auch in späteren Phasen des Lebens durch Erfahrungen modifizierbar. Welche Auswirkungen negative Lebensereignisse auf die Entwicklung des Angstphänotyps haben, wird allerdings maßgeblich durch die genetische Disposition des Individuums bestimmt. Besonders gut sind diese Zusammenhänge am Beispiel eines Polymorphismus untersucht, der die Funktion des Serotonintransporter-Gens moduliert. Deshalb fokussiert dieser Übersichtsartikel auf dieses Kandidatengen, um das Zusammenspiel von Genotyp und Umwelt bei der Entwicklung von Furcht und Angst zu erhellen.}, author = {Sachser, Norbert and Lesch, Klaus-Peter}, doi = {10.1515/nf-2013-0304}, journal = {e-Neuroforum}, month = {jan}, pages = {104-109}, title = {Das Zusammenspiel von Genotyp und Umwelt bei der Entwicklung von Furcht und Angst}, url = {http://www.degruyter.com/downloadpdf/j/nf.2013.19.issue-3/nf-2013-0304/nf-2013-0304.xml}, volume = {19}, year = {2013} } @article{Waider2012, author = {Waider, Jonas and Proft, Florian and Langlhofer, Georg and Asan, Esther and Lesch, Klaus-Peter and Gutknecht, Lise}, doi = {10.1007/s00418-012-1029-x}, journal = {Histochemistry and Cell Biology}, month = {oct}, pages = {267-281}, title = {GABA concentration and GABAergic neuron populations in limbic areas are differentially altered by brain serotonin deficiency in Tph2 knockout mice}, url = {https://oadoi.org/10.1007/s00418-012-1029-x}, volume = {139}, year = {2012} }