Dr. Marion Rivalan

Die Forschung von Dr. Marion Rivalan konzentriert sich auf die neurowissenschaftlichen Grundlagen des Verhaltens, insbesondere die Rolle von Serotonin bei Aggression, sozialer Interaktion und Entscheidungsfindung. Sie entwickelt und wendet innovative Methoden wie Home-Cage-Monitoring (HCM) an, um Tierverhalten in halbnatürlichen Umgebungen longitudinal zu erfassen und so die ökologische Validität von Präklinika-Studien zu erhöhen. Ein weiterer Schwerpunkt liegt auf der Analyse geschlechtsspezifischer Unterschiede in neurochemischen Prozessen und Verhaltensmustern, etwa im Kontext von Alkoholabhängigkeit und Essverhalten. Durch den Einsatz von Machine Learning und elektrophysiologischen Techniken verbindet sie molekularbiologische Erkenntnisse mit komplexen Verhaltensphänotypen. Ihr Ziel ist die Verbesserung der Translationalität von tierexperimentellen Daten für die Erforschung psychischer Erkrankungen.

🔒 Das System hat 710 mögliche Industrie-Partner gefunden — Firmen, Scores und Begründungen sind nur für eingeloggte Nutzer:innen sichtbar. Anmelden

• Multidimensional Description of Behavioural Phenotypes: Role of Serotonine in Individual Profiles of Behaviour

  Quelle ↗

  Förderer: DFG Sachbeihilfe Zeitraum: 05/2015 - 04/2019 Projektleitung: Dr. Marion Rivalan

• Risk-Prone Individuals Prefer the Wrong Options on a Rat Version of the Iowa Gambling Task

  2009

  Biological Psychiatry · DOI

• Evidence for the role of corticotropin-releasing factor in major depressive disorder

  2015

  Neuroscience & Biobehavioral Reviews · DOI

• Human gestational <i>N</i>‐methyl‐<scp>d</scp>‐aspartate receptor autoantibodies impair neonatal murine brain function

  2019

  Annals of Neurology · DOI

  OBJECTIVE: Maternal autoantibodies are a risk factor for impaired brain development in offspring. Antibodies (ABs) against the NR1 (GluN1) subunit of the N-methyl-d-aspartate receptor (NMDAR) are among the most frequently diagnosed anti-neuronal surface ABs, yet little is known about effects on fetal development during pregnancy. METHODS: We established a murine model of in utero exposure to human recombinant NR1 and isotype-matched nonreactive control ABs. Pregnant C57BL/6J mice were intraperitoneally injected on embryonic days 13 and 17 each with 240μg of human monoclonal ABs. Offspring were investigated for acute and chronic effects on NMDAR function, brain development, and behavior. RESULTS: Transferred NR1 ABs enriched in the fetus and bound to synaptic structures in the fetal brain. Density of NMDAR was considerably reduced (up to -49.2%) and electrophysiological properties were altered, reflected by decreased amplitudes of spontaneous excitatory postsynaptic currents in young neonates (-34.4%). NR1 AB-treated animals displayed increased early postnatal mortality (+27.2%), impaired neurodevelopmental reflexes, altered blood pH, and reduced bodyweight. During adolescence and adulthood, animals showed hyperactivity (+27.8% median activity over 14 days), lower anxiety, and impaired sensorimotor gating. NR1 ABs caused long-lasting neuropathological effects also in aged mice (10 months), such as reduced volumes of cerebellum, midbrain, and brainstem. INTERPRETATION: The data collectively support a model in which asymptomatic mothers can harbor low-level pathogenic human NR1 ABs that are diaplacentally transferred, causing neurotoxic effects on neonatal development. Thus, AB-mediated network changes may represent a potentially treatable neurodevelopmental congenital brain disorder contributing to lifelong neuropsychiatric morbidity in affected children. ANN NEUROL 2019;86:656-670.