error
Kurzer Serviceunterbruch am Donnerstag, 22. Januar 2026, 12 bis 13 Uhr. Sie können in diesem Zeitraum keine neuen Dokumente hochladen oder bestehende Einträge bearbeiten. Das Login wird in diesem Zeitraum deaktiviert. Grund: Wartungsarbeiten // Short service interruption on Thursday, January 22, 2026, 12.00 – 13.00. During this time, you won’t be able to upload new documents or edit existing records. The login will be deactivated during this time. Reason: maintenance work
 

Journal: Neuropsychopharmacology

Abbreviation

Neuropsychopharmacol.

Publisher

Springer

Journal Volumes

ISSN

0893-133X
1740-634X

Description

Filters

2021 - 20223
Reset filters

Search Results

Publications 1 - 3 of 3
  • A versatile GPCR toolkit to track in vivo neuromodulation: not a one-size-fits-all sensor
    Item type: Other Journal Item
    Labouesse, Marie A.; Patriarchi, Tommaso (2021)
    Neuropsychopharmacology
  • Opioid-blunted cortisol response to stress is associated with increased negative mood and wanting of social reward
    Item type: Journal Article
    Massaccesi, Claudia; Willeit, Matthaeus; Quednow, Boris B.; et al. (2022)
    Neuropsychopharmacology
    Animal research suggests a central role of the mu-opioid receptor (MOR) system in regulating affiliative behaviors and in mediating the stress-buffering function of social contact. However, the neurochemistry of stress-related social contact seeking in humans is still poorly understood. In a randomized, double-blind, between-subjects design, healthy female volunteers (N = 80) received either 10 mg of the mu-opioid agonist morphine sulfate, or a placebo. Following a standardized psychosocial stress induction, participants engaged in a social reward task, in which the motivation to obtain skin-to-skin social touch and the hedonic reactions elicited by such touch were assessed. Morphine prevented the increase of salivary cortisol typically observed following acute stress exposure. Notably, this altered HPA axis responsivity was associated with increased negative affect in response to psychosocial stress, and with enhanced subjective wanting of highly rewarding social contact. These findings provide novel evidence on the effect of exogenous opioids administration on the reactions to psychosocial stress and point to a state-dependent regulation of social motivation.
  • Symptomatic and preventive effects of the novel phosphodiesterase-9 inhibitor BI 409306 in an immune-mediated model of neurodevelopmental disorders
    Item type: Journal Article
    Scarborough, Joseph; Mattei, Daniele; Dorner-Ciossek, Cornelia; et al. (2021)
    Neuropsychopharmacology
    BI 409306, a phosphodiesterase-9 inhibitor under development for treatment of schizophrenia and attenuated psychosis syndrome (APS), promotes synaptic plasticity and cognition. Here, we explored the effects of BI 409306 treatment in the polyriboinosinic-polyribocytidilic acid (poly[I:C])-based mouse model of maternal immune activation (MIA), which is relevant to schizophrenia and APS. In Study 1, adult offspring received BI 409306 0.2, 0.5, or 1 mg/kg or vehicle to establish an active dose. In Study 2, adult offspring received BI 409306 1 mg/kg and/or risperidone 0.025 mg/kg, risperidone 0.05 mg/kg, or vehicle, to evaluate BI 409306 as add-on to standard therapy for schizophrenia. In Study 3, offspring received BI 409306 1 mg/kg during adolescence only, or continually into adulthood to evaluate preventive effects of BI 409306. We found that BI 409306 significantly mitigated MIA-induced social interaction deficits and amphetamine-induced hyperlocomotion, but not prepulse inhibition impairments, in a dose-dependent manner (Study 1). Furthermore, BI 409306 1 mg/kg alone or in combination with risperidone 0.025 mg/kg significantly reversed social interaction deficits and attenuated amphetamine-induced hyperlocomotion in MIA offspring (Study 2). Finally, we revealed that BI 409306 1 mg/kg treatment restricted to adolescence prevented adult deficits in social interaction, whereas continued treatment into adulthood also significantly reduced amphetamine-induced hyperlocomotion (Study 3). Taken together, our findings suggest that symptomatic treatment with BI 409306 can restore social interaction deficits and dopaminergic dysfunctions in a MIA model of neurodevelopmental disruption, lending preclinical support to current clinical trials of BI 409306 in patients with schizophrenia. Moreover, BI 409306 given during adolescence has preventive effects on adult social interaction deficits in this model, supporting its use in people with APS.
Publications 1 - 3 of 3