Although many high-risk studies have focused on impairments in neurocognitive functions, such as memory
and attention, very few studies have investigated problems in processing social cues such as facial expressions as a possible vulnerability marker for psychosis.
Method. Thirty-six adolescents at ultra-high risk (UHR) for psychosis and 21 non-clinical controls completed a face recognition test, a facial affect labeling test and an inhibitory control test. Schizotypal traits and schizophrenia symptoms were assessed using a schizotypy questionnaire and the Positive and Negative Syndrome Scale (PANSS).
Results. The UHR group showed impairments in labeling facial expressions of others, in addition to a spared selleck screening library ability to recognize facial identity. More specifically, the UHR group made more errors in labeling neutral expressions compared to the controls, learn more and an analysis of error types indicated that neutral faces were misattributed as being angry.
The degree of misattribution of neutral-as-angry faces correlated significantly with reduced inhibitory control.
Conclusions. Our findings suggest that misattributing social cues might contribute to vulnerability for psychosis. This social cognitive deficit may be related to problems in inhibitory control, which potentially plays an important role in the selection of appropriate social meaning. These findings may have relevance for understanding the mechanisms underlying prodromal social dysfunction, which should be targeted in future remediation interventions.”
“Depressive disorders have been linked to the combined dysregulation of the hypothalamus-pituitary-adrenal MK5108 supplier (HPA)-axis and the serotonergic system. The HPA-axis
and serotonergic (5-HT) neurons exert reciprocal regulatory actions. It has been reported that glucocorticoid-glucocorticoid receptor (GR) signaling influences serotonin transporter (5-HTT) transcription but data also points to the fact that 5-HTT expression is regulated nongenomically via redistribution of 5-HTT from the cell surface into intracellular compartments. In order to analyze the acute effects of glucocorticoids on 5-HTT cell surface localization we differentiated serotonergic neurons from mouse embryonic stem (ES) cells derived from the C57BL/6N blastocysts. These postmitotic 5-HT neurons express all relevant serotonergic markers following the application of a growth factor-based differentiation protocol. Increasing concentrations of the GR agonist dexamethasone (Dex) resulted in enhanced, dose-dependent 5-HTT cell surface localization in the presence of the protein synthesis inhibitor cycloheximide already 1 h after incubation. Inhibition of GR function by the specific GR-antagonist mifepristone abolished the increase in 5-HTT cell surface localization.