TY - JOUR A1 - Muzerelle, Aude A1 - Soiza-Reilly, Mariano A1 - Hainer, Cornelia A1 - Ruet, Pierre-Louis A1 - Lesch, Klaus-Peter A1 - Bader, Michael A1 - Alenina, Natalia A1 - Scotto-Lomassese, Sophie A1 - Gaspar, Patricia T1 - Dorsal raphe serotonin neurotransmission is required for the expression of nursing behavior and for pup survival JF - Scientific Reports N2 - Proper maternal care is an essential factor of reproductive success in mammals, involving a repertoire of behaviors oriented toward the feeding and care of the offspring. Among the neurotransmitters involved in the initiation of these behaviors, serotonin (5-HT) seems to play an important role. Here we compared pup-oriented maternal behaviors in mice with constitutive 5-HT depletion, the tryptophan hydroxylase 2-knock-out (Tph2-KO) and the Pet1-KO mice. We report that the only common pup-oriented defect in these 2 hyposerotoninergic models is a defective nursing in parturient mice and altered nursing-like (crouching) behavior in virgin mice, while pup retrieval defects are only present in Tph2-KO. Despite a normal mammary gland development and milk production, the defect in appropriate nursing is responsible for severe growth retardation and early lethality of pups born to hyposerotonergic dams. This nursing defect is due to acute rather constitutive 5-HT depletion, as it is reproduced by adult knockdown of Tph2 in the dorsal raphe nucleus in mothers with a prior normal maternal experience. We conclude that 5-HT innervation from the dorsal raphe is required for both the initiation and maintenance of a normal nursing behavior. Our findings may be related to observations of reduced maternal/infant interactions in human depression. Y1 - 2021 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-371501 VL - 11 ER - TY - JOUR A1 - Mossink, Britt A1 - van Rhijn, Jon-Ruben A1 - Wang, Shan A1 - Linda, Katrin A1 - Vitale, Maria R. A1 - Zöller, Johanna E. M A1 - van Hugte, Eline J. H. A1 - Bak, Jitske A1 - Verboven, Anouk H. A. A1 - Selten, Martijn A1 - Negwer, Moritz A1 - Latour, Brooke L. A1 - van der Werf, Ilse A1 - Keller, Jason M. A1 - Klein Gunnewiek, Teun M. A1 - Schoenmaker, Chantal A1 - Oudakker, Astrid A1 - Anania, Alessia A1 - Jansen, Sophie A1 - Lesch, Klaus-Peter A1 - Frega, Monica A1 - van Bokhoven, Hans A1 - Schubert, Dirk A1 - Kasri, Nael Nadif T1 - Cadherin-13 is a critical regulator of GABAergic modulation in human stem-cell-derived neuronal networks JF - Molecular Psychiatry N2 - Activity in the healthy brain relies on a concerted interplay of excitation (E) and inhibition (I) via balanced synaptic communication between glutamatergic and GABAergic neurons. A growing number of studies imply that disruption of this E/I balance is a commonality in many brain disorders; however, obtaining mechanistic insight into these disruptions, with translational value for the patient, has typically been hampered by methodological limitations. Cadherin-13 (CDH13) has been associated with autism and attention-deficit/hyperactivity disorder. CDH13 localizes at inhibitory presynapses, specifically of parvalbumin (PV) and somatostatin (SST) expressing GABAergic neurons. However, the mechanism by which CDH13 regulates the function of inhibitory synapses in human neurons remains unknown. Starting from human-induced pluripotent stem cells, we established a robust method to generate a homogenous population of SST and MEF2C (PV-precursor marker protein) expressing GABAergic neurons (iGABA) in vitro, and co-cultured these with glutamatergic neurons at defined E/I ratios on micro-electrode arrays. We identified functional network parameters that are most reliably affected by GABAergic modulation as such, and through alterations of E/I balance by reduced expression of CDH13 in iGABAs. We found that CDH13 deficiency in iGABAs decreased E/I balance by means of increased inhibition. Moreover, CDH13 interacts with Integrin-β1 and Integrin-β3, which play opposite roles in the regulation of inhibitory synaptic strength via this interaction. Taken together, this model allows for standardized investigation of the E/I balance in a human neuronal background and can be deployed to dissect the cell-type-specific contribution of disease genes to the E/I balance. Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-371170 VL - 27 ER - TY - JOUR A1 - Andreatta, Marta A1 - Pauli, Paul T1 - Generalization of appetitive conditioned responses JF - Psychophysiology N2 - A stimulus (conditioned stimulus, CS) associated with an appetitive unconditioned stimulus (US) acquires positive properties and elicits appetitive conditioned responses (CR). Such associative learning has been examined extensively in animals with food as the US, and results are used to explain psychopathologies (e.g., substance-related disorders or obesity). Human studies on appetitive conditioning exist, too, but we still know little about generalization processes. Understanding these processes may explain why stimuli not associated with a drug, for instance, can elicit craving. Forty-seven hungry participants underwent an appetitive conditioning protocol during which one of two circles with different diameters (CS+) became associated with an appetitive US (chocolate or salty pretzel, according to participants’ preference) but never the other circle (CS−). During generalization, US were delivered twice and the two CS were presented again plus four circles (generalization stimuli, GS) with gradually increasing diameters from CS− to CS+. We found successful appetitive conditioning as reflected in appetitive subjective ratings (positive valence, higher contingency) and physiological responses (startle attenuation and larger skin conductance responses) to CS+ versus CS−, and, importantly, both measures confirmed generalization as indicated by generalization gradients. Small changes in CS-US contingency during generalization may have weakened generalization processes on the physiological level. Considering that appetitive conditioned responses can be generalized to non-US-associated stimuli, a next important step would be to investigate risk factors that mediate overgeneralization. KW - appetitive conditioning; ; KW - generalization KW - primary reinforcer KW - startle reflex Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-221132 VL - 56 ER - TY - THES A1 - Kußberger, Julia Bettina T1 - Protein - Biomarker zur Unterscheidung zwischen unipolarer und bipolarer Depression T1 - Protein - Biomarkers for Differentiating Between Unipolar and Bipolar Depression N2 - Die Diagnosestellung von unipolarer und bipolarer Depression basiert bis heute ausschließlich auf der Bewertung klinischer Symptome. Objektive biochemische Marker, wie sie bei zahlreichen somatischen Krankheiten zur Diagnosestellung angewendet werden, sind bisher nicht verfügbar. Da sich die beide Krankheitsbilder vor allem in der depressiven Episode stark ähneln, ist eine Unterscheidung in diesem Krankheitsstadium häufig nicht eindeutig möglich. Dies kann zu Fehldiagnosen, einer Verschlechterung des Krankheitsverlaufs, einer erhöhten Krankheitslast und höheren Gesundheitskosten führen. Periphere Biomarker wären daher wertvoll, um die klinische Diagnosestellung zu unterstützen und eine adäquate Behandlung frühzeitige zu ermöglichen. In einer vorherigen Studie der Arbeitsgruppe haben Proteom-Analysen bestimmte Proteine wie den Wachstumsfaktor PDGF-BB und das Thrombospondin TSP-1 identifiziert, die potenziell als Biomarker fungieren könnten. In der vorliegenden Studie wurde untersucht, ob sich die Konzentration von PDGF-BB und TSP-1 im Blut zwischen Patient*innen mit unipolarer bzw. bipolarer Depression signifikant unterscheidet. Es konnte gezeigt werden, dass PDGF-BB bei unipolaren Patientinnen signifikant niedriger ist als bei bipolaren Patientinnen und gesunden Kontrollpersonen. Zudem sank die PDGF-BB-Konzentration bei bipolaren Patientinnen während einer remittierten Episode im Vergleich zu einer depressiven Episode signifikant ab. Im Gegensatz dazu zeigte TSP-1 keine signifikanten Unterschiede zwischen den Patient*innengruppen und Kontrollpersonen. Die Arbeit konnte zeigen, dass PDGF-BB das Potenzial hat, als diagnostischer Biomarker für die Unterscheidung zwischen unipolarer und bipolarer Depression zu dienen, während TSP-1 in dieser Hinsicht nicht geeignet erscheint. Weitere Forschung ist jedoch notwendig, um die Rolle von PDGF-BB in der Pathogenese affektiver Erkrankungen besser zu verstehen und seinen Einsatz als Biomarker im klinischen Alltag zu validieren.   N2 - The diagnosis of unipolar and bipolar depression is still based on clinical symptoms. Objective biochemical markers, which are commonly used for diagnosing somatic diseases, are not yet available. Since both conditions, particularly during the depressive phase, exhibit very similar symptoms, distinguishing between them in this stage is often complicated. This can lead to misdiagnosis, a worsening of the disease course, increased disease burden, and higher healthcare costs. Peripheral biomarkers would therefore be of great value in supporting clinical diagnosis and enabling early and appropriate treatment. A previous study by our research group identified proteins such as the growth factor PDGF-BB and thrombospondin TSP-1 through proteomic analysis, which could potentially serve as biomarkers. In the present study, the concentrations of PDGF-BB and TSP-1 in the blood of patients with unipolar and bipolar depression were examined to determine if there were significant differences. The results showed that PDGF-BB levels were significantly lower in unipolar patients compared to bipolar patients and healthy controls. Additionally, PDGF-BB concentrations decreased significantly in bipolar patients during a remitted episode compared to a depressive episode. In contrast, TSP-1 did not show significant differences between the groups studied. The study suggests that PDGF-BB has the potential to serve as a diagnostic biomarker for differentiating between unipolar and bipolar depression, whereas TSP-1 appears less suitable in this context. However, further research is needed to better understand the role of PDGF-BB in the pathogenesis of affective disorders and to validate its clinical utility as a biomarker. KW - Differentialdiagnose KW - Depression KW - Biomarker KW - Affektive Erkrankungen Y1 - 2024 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-371109 ER - TY - JOUR A1 - Kiser, Dominik P. A1 - Popp, Sandy A1 - Schmitt-Böhrer, Angelika G. A1 - Strekalova, Tatyana A1 - van den Hove, Daniel L. A1 - Lesch, Klaus-Peter A1 - Rivero, Olga T1 - Early-life stress impairs developmental programming in Cadherin 13 (CDH13)-deficient mice JF - Progress in Neuropsychopharmacology & Biological Psychiatry N2 - Objective Cadherin-13 (CDH13), a member of the calcium-dependent cell adhesion molecule family, has been linked to neurodevelopmental disorders, including autism spectrum (ASD) and attention-deficit/hyperactivity (ADHD) disorders, but also to depression. In the adult brain, CDH13 expression is restricted e.g. to the presynaptic compartment of inhibitory GABAergic synapses in the hippocampus and Cdh13 knockout mice show an increased inhibitory drive onto hippocampal CA1 pyramidal neurons, leading to a shift in excitatory/inhibitory balance. CDH13 is also moderating migration of serotonergic neurons in the dorsal raphe nucleus, establishing projections preferentially to the thalamus and cerebellum during brain development. Furthermore, CDH13 is upregulated by chronic stress as well as in depression, suggesting a role in early-life adaptation to stressful experience. Here, we therefore investigated the interaction between Cdh13 variation and neonatal maternal separation (MS) in mice. Methods Male and female wild-type (Cdh13+/+), heterozygous (Cdh13+/−) and homozygous (Cdh13−/−) knockout mice exposed to MS, or daily handling as control, were subjected to a battery of behavioural tests to assess motor activity, learning and memory as well as anxiety-like behaviour. A transcriptome analysis of the hippocampus was performed in an independent cohort of mice which was exposed to MS or handling, but remained naïve for behavioural testing. Results MS lead to increased anxiety-like behaviour in Cdh13−/− mice compared to the other two MS groups. Cdh13−/− mice showed a context-dependent effect on stress- and anxiety-related behaviour, impaired extinction learning following contextual fear conditioning and decreased impulsivity, as well as a mild decrease in errors in the Barnes maze and reduced risk-taking in the light-dark transition test after MS. We also show sex differences, with increased locomotor activity in female Cdh13−/− mice, but unaltered impulsivity and activity in male Cdh13−/− mice. Transcriptome analysis revealed several pathways associated with cell surface/adhesion molecules to be altered following Cdh13 deficiency, together with an influence on endoplasmic reticulum function. Conclusion MS resulted in increased stress resilience, increased exploration and an overall anxiolytic behavioural phenotype in male Cdh13+/+ and Cdh13+/− mice. Cdh13 deficiency, however, obliterated most of the effects caused by early-life stress, with Cdh13−/− mice exhibiting delayed habituation, no reduction of anxiety-like behaviour and decreased fear extinction. Our behavioural findings indicate a role of CDH13 in the programming of and adaptation to early-life stress. Finally, our transcriptomic data support the view of CDH13 as a neuroprotective factor as well as a mediator in cell-cell interactions, with an impact on synaptic plasticity. KW - Cadherin-13 (CDH13) KW - T-cadherin KW - neurodevelopment KW - autism KW - ADHD KW - depression KW - psychiatric disorders KW - early-life stress KW - mouse KW - RNA sequencing KW - endoplasmic reticulum stress KW - adhesion Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-325859 VL - 89 ER - TY - JOUR A1 - Argyrousi, Elentina K. A1 - de Nijs, Laurence A1 - Lagatta, Davi C. A1 - Schlütter, Anna A1 - Weidner, Magdalena T. A1 - Zöller, Johanna A1 - van Goethem, Nick P. A1 - Joca, Sâmia R. L. A1 - van den Hove, Daniel L. A. A1 - Prickaerts, Jos T1 - Effects of DNA methyltransferase inhibition on pattern separation performance in mice JF - Neurobiology of Learning and Memory N2 - Enhancement of synaptic plasticity through changes in neuronal gene expression is a prerequisite for improved cognitive performance. Moreover, several studies have shown that DNA methylation is able to affect the expression of (e.g. plasticity) genes that are important for several cognitive functions. In this study, the effect of the DNA methyltransferase (DNMT) inhibitor RG108 was assessed on object pattern separation (OPS) task in mice. In addition, its effect on the expression of target genes was monitored. Administration of RG108 before the test led to a short-lasting, dose-dependent increase in pattern separation memory that was not present anymore after 48 h. Furthermore, treatment with RG108 did not enhance long-term memory of the animals when tested after a 24 h inter-trial interval in the same task. At the transcriptomic level, acute treatment with RG108 was accompanied by increased expression of Bdnf1, while expression of Bdnf4, Bdnf9, Gria1 and Hdac2 was not altered within 1 h after treatment. Methylation analysis of 14 loci in the promoter region of Bdnf1 revealed a counterintuitive increase in the levels of DNA methylation at three CpG sites. Taken together, these results indicate that acute administration of RG108 has a short-lasting pro-cognitive effect on object pattern separation that could be explained by increased Bdnf1 expression. The observed increase in Bdnf1 methylation suggests a complex interplay between Bdnf methylation-demethylation that promotes Bdnf1 expression and associated cognitive performance. Considering that impaired pattern separation could constitute the underlying problem of a wide range of mental and cognitive disorders, pharmacological agents including DNA methylation inhibitors that improve pattern separation could be compelling targets for the treatment of these disorders. In that respect, future studies are needed in order to determine the effect of chronic administration of such agents. KW - object pattern separation KW - DNA methyltransferase inhibitors KW - BDNF KW - CpG islands KW - epigenetics KW - hippocampal plasticity Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-221226 VL - 159 ER - TY - JOUR A1 - Figel, Benedikt A1 - Brinkmann, Leonie A1 - Buff, Christine A1 - Heitmann, Carina Y. A1 - Hofmann, David A1 - Bruchmann, Maximilian A1 - Becker, Michael P. I. A1 - Herrmann, Martin J. A1 - Straube, Thomas T1 - Phasic amygdala and BNST activation during the anticipation of temporally unpredictable social observation in social anxiety disorder patients JF - NeuroImage: Clinical N2 - Anticipation of potentially threatening social situations is a key process in social anxiety disorder (SAD). In other anxiety disorders, recent research of neural correlates of anticipation of temporally unpredictable threat suggests a temporally dissociable involvement of amygdala and bed nucleus of the stria terminalis (BNST) with phasic amygdala responses and sustained BNST activation. However, the temporal profile of amygdala and BNST responses during temporal unpredictability of threat has not been investigated in patients suffering from SAD. We used functional magnetic resonance imaging (fMRI) to investigate neural activation in the central nucleus of the amygdala (CeA) and the BNST during anticipation of temporally unpredictable aversive (video camera observation) relative to neutral (no camera observation) events in SAD patients compared to healthy controls (HC). For the analysis of fMRI data, we applied two regressors (phasic/sustained) within the same model to detect temporally dissociable brain responses. The aversive condition induced increased anxiety in patients compared to HC. SAD patients compared to HC showed increased phasic activation in the CeA and the BNST for anticipation of aversive relative to neutral events. SAD patients as well as HC showed sustained activity alterations in the BNST for aversive relative to neutral anticipation. No differential activity during sustained threat anticipation in SAD patients compared to HC was found. Taken together, our study reveals both CeA and BNST involvement during threat anticipation in SAD patients. The present results point towards potentially SAD-specific threat processing marked by elevated phasic but not sustained CeA and BNST responses when compared to HC. KW - FMRI KW - threat anticipation KW - social anxiety disorder KW - bed nucleus of stria terminalis KW - amygdala Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-228071 VL - 22 ER - TY - JOUR A1 - Gorlova, Anna A1 - Pavlov, Dmitrii A1 - Anthony, Daniel C. A1 - Ponomarev, Eugene D. A1 - Sambon, Margaux A1 - Proshin, Andrey A1 - Shafarevich, Igor A1 - Babaevskaya, Diana A1 - Lesch, Klaus-Peter A1 - Bettendorff, Lucien A1 - Strekalova, Tatyana T1 - Thiamine and benfotiamine counteract ultrasound-induced aggression, normalize AMPA receptor expression and plasticity markers, and reduce oxidative stress in mice JF - Neuropharmacology N2 - The negative societal impacts associated with the increasing prevalence of violence and aggression is increasing, and, with this rise, is the need to understand the molecular and cellular changes that underpin ultrasound-induced aggressive behavior. In mice, stress-induced aggression is known to alter AMPA receptor subunit expression, plasticity markers, and oxidative stress within the brain. Here, we induced aggression in BALB/c mice using chronic ultrasound exposure and examined the impact of the psychoactive anti-oxidant compounds thiamine (vitamin B1), and its derivative benfotiamine, on AMPA receptor subunit expression, established plasticity markers, and oxidative stress. The administration of thiamine or benfotiamine (200 mg/kg/day) in drinking water decreased aggressive behavior following 3-weeks of ultrasound exposure and benfotiamine, reduced floating behavior in the swim test. The vehicle-treated ultrasound-exposed mice exhibited increases in protein carbonyl and total glutathione, altered AMPA receptor subunits expression, and decreased expression of plasticity markers. These ultrasound-induced effects were ameliorated by thiamine and benfotiamine treatment; in particular both antioxidants were able to reverse ultrasound-induced changes in GluA1 and GluA2 subunit expression, and, within the prefrontal cortex, significantly reversed the changes in protein carbonyl and polysialylated form of neural cell adhesion molecule (PSA-NCAM) expression levels. Benfotiamine was usually more efficacious than thiamine. Thus, the thiamine compounds were able to counteract ultrasound-induced aggression, which was accompanied by the normalization of markers that have been showed to be associated with ultrasound-induced aggression. These commonly used, orally-active compounds may have considerable potential for use in the control of aggression within the community. This article is part of the Special Issue entitled ‘Current status of the neurobiology of aggression and impulsivity’. KW - aggression KW - emotional stress KW - brain oxidative stress KW - plasticity KW - thiamine KW - mice Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-227439 VL - 156 ER - TY - JOUR A1 - Verheijen, Bert M. A1 - Stevens, Jo A. A. A1 - Gentier, Romina J. G. A1 - van't Hekke, Christian D. A1 - van den Hove, Daniel L. A. A1 - Hermes, Denise J. H. P. A1 - Steinbusch, Harry W. M. A1 - Ruijter, Jan M. A1 - Grimm, Marcus O. W. A1 - Haupenthal, Viola J. A1 - Annaert, Wim A1 - Hartmann, Tobias A1 - van Leeuwen, Fred W. T1 - Paradoxical effects of mutant ubiquitin on Aβ plaque formation in an Alzheimer mouse model JF - Neurobiology of Aging N2 - Amyloid-β (Aβ) plaques are a prominent pathological hallmark of Alzheimer's disease (AD). They consist of aggregated Aβ peptides, which are generated through sequential proteolytic processing of the transmembrane protein amyloid precursor protein (APP) and several Aβ-associated factors. Efficient clearance of Aβ from the brain is thought to be important to prevent the development and progression of AD. The ubiquitin-proteasome system (UPS) is one of the major pathways for protein breakdown in cells and it has been suggested that impaired UPS-mediated removal of protein aggregates could play an important role in the pathogenesis of AD. To study the effects of an impaired UPS on Aβ pathology in vivo, transgenic APPSwe/PS1ΔE9 mice (APPPS1) were crossed with transgenic mice expressing mutant ubiquitin (UBB+1), a protein-based inhibitor of the UPS. Surprisingly, the APPPS1/UBB+1 crossbreed showed a remarkable decrease in Aβ plaque load during aging. Further analysis showed that UBB+1 expression transiently restored PS1-NTF expression and γ-secretase activity in APPPS1 mice. Concurrently, UBB+1 decreased levels of β-APP-CTF, which is a γ-secretase substrate. Although UBB+1 reduced Aβ pathology in APPPS1 mice, it did not improve the behavioral deficits in these animals. KW - mutant ubiquitin KW - ubiquitin-proteasome system KW - γ-secretase KW - amyloid-β KW - behavior KW - Alzheimer's disease Y1 - 2018 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-233185 VL - 72 ER - TY - THES A1 - Adolf, Jonas Michael T1 - Die Zusammenarbeit zwischen der stationären beziehungsweise teilstationären psychotherapeutischen Behandlung und niedergelassenen Psychotherapeut:innen T1 - The Collaboration between inpatient and semi-inpatient psychotherapeutic treatment and outpatient psychotherapists N2 - Das Ziel der vorliegenden Arbeit war es die aktuelle Versorgungskontinuität in der psychotherapeutischen Versorgung hinsichtlich der Zusammenarbeit des (teil-)stationären und des ambulanten Sektors aus Sicht der niedergelassenen Psychotherapeut:innen zu untersuchen, diese in den wissenschaftlichen Kontext einzuordnen und – falls möglich – erste Möglichkeiten zur Verbesserung der derzeitigen Versorgungskontinuität aufzuzeigen. In Zusammenarbeit mit dem Arbeitsbereich für Medizinische Psychologie und Psychotherapie im Zentrum für psychische Gesundheit des Universitätsklinikums Würzburg wurde hierzu ein Fragebogen entwickelt und acht ausgewählten psychotherapeutischen Fachgesellschaften beziehungsweise Psychotherapeutenkammern mit der Bitte um Weiterleitung an deren Mitglieder zugesandt. In der vorliegenden Studie wurden – neben einer Globalbeurteilung – im Speziellen die Teil-aspekte des Austauschs, der entsprechenden Rahmenbedingungen und die Bereitstellung des poststationären ambulanten Psychotherapieplatzes betrachtet. Die Studienergebnisse bilden den derzeitigen Status Quo der psychotherapeutischen Versorgungslage aus Sicht der niedergelassenen Psychotherapeut:innen ab und weisen im Zuge dessen auf einige Defizite in den untersuchten Teilaspekten hin. Die aufgestellten Nebenfragestellungen zeigen gleichsam aber auch Ansatzunkte für Lösungen auf. Aufgrund der besonderen Relevanz der aufgezeigten Ergebnisse, gilt es – zur Ermöglichung einer adäquaten kontinuierlichen psychotherapeutischen Versorgung – eine weitergehende Betrach-tung der aufgezeigten Defizite vorzunehmen. Für ein umfassendes Bild sind zudem kongruente Folgearbeiten mit dem Augenmerk auf der Sichtweise der (teil-)stationären Behandlungseinrichtungen und der Patient:innen notwendig. Insbesondere vor dem Hintergrund der limitierten Möglichkeiten der vorliegenden Arbeit gilt es große repräsentative und nationale Studien anzustreben. Hierzu wäre die Etablierung zentral verwalteter Register zur Bündelung der bisherigen und zukünftigen Forschungsarbeiten im Bereich der Psychotherapie wünschenswert. Vor allem vor dem Hintergrund zahlreicher Modellprojekte erscheint dies sinnvoll und könnte einen wichtigen Beitrag zur Optimierung der derzeitigen psychotherapeutischen Forschungs- und Versorgungslage beitragen. N2 - The aim of the study was to identify the current continuity of care regarding psychotherapeutic care and the collaboration of the (semi-)inpatient and outpatient field from point of view of the outpatient psychotherapists. Furthermore, the study wants to integrate the findings in the recent scientific context and wants to reveal improvements regarding the continuity of care in the field of psychotherapy. An explorative survey was created in collaboration with the working group of medical psychology and psychotherapy at the centre for mental health of the university hospital of Würzburg. Eight selected psychotherapeutic organisations (psychotherapy chambers and societies) were invited to conduct the survey to their members. Apart from a general assessment the study took a closer look at the framework conditions, the field of exchange and the care of outpatient psychotherapy to patients after (semi-)inpatient care. The study results describe the current situation of the psychotherapy care in Germany from the point of view of the outpatient psychotherapists and demonstrate on the one hand deficits regarding the analysed aspects and – as part of the side questions – on the other hand possible approaches for improvements. To facilitate a better continuity of psychotherapeutic care, it is important to take a closer look at the demonstrated deficits reported by the study. Moreover further studies are necessary treating the point of view of (semi-)inpatient psychotherapists as well as to conduct large national-wide representative studies, especially against the backdrop of the limited possibilities of the present study. For this purpose, it is helpful to establish a central-managed register to collect all studies in the field of psychotherapy. That could contribute to improve the current situation of research and care in the field of psychotherapy, in particular against the backdrop of the numerous pilot projects. KW - Psychotherapie KW - Medizinische Versorgung KW - Versorgungskontinuität KW - Sektoren KW - Versorgung KW - Psychiatrie Y1 - 2024 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-371098 ER -