Facial Feedback in Implicit Sequence Learning

There is continuous debate how closely or loosely emotion is linked to behavior and especially to facial expressions. In strong versions of the so-called facial feedback hypothesis, it is assumed that facial activity can intensify, modulate and initiate emotions. The hypothesis has been largely investigated with various emotions, however, surprise was tested only in a few studies. Additionally, it has been discussed frequently how obtrusively manipulations of facial feedback as well as the dependent measures are. Thus, in the present experiment we analyzed whether unobtrusive facial feedback of surprise versus no-surprise can modulate reactions following deviations in an implicit sequence learning task. Participants had to quickly and accurately press keys which corresponded to one of four letters appearing at the screen. After several blocks in which a standard sequence (consisting of a predefined order of 12 letters) was repeated, standard sequences and deviation sequences (i.e. one element differed from the standard sequence) were intermixed. The results confirmed our hypothesis: Participants of the surprise face condition showed longer reaction times to deviation sequences than to standard sequences. In contrast, participants of the no-surprise face condition did not show this difference in reaction times. Results were discussed with respect to implicit learning as well as to theories on emotion and facial feedback taking the special status of surprise into account (AU)

No disponible

Parkin mediates neuroprotection through activation of IkappaB kinase/nuclear factor-kappaB signaling.

Mutations in the parkin gene are a major cause of autosomal recessive Parkinson's disease. Here we show that the E3 ubiquitin ligase parkin activates signaling through the IkappaB kinase (IKK)/nuclear factor kappaB (NF-kappaB) pathway. Our analysis revealed that activation of this signaling cascade is causally linked to the neuroprotective potential of parkin. Inhibition of NF-kappaB activation by an IkappaB super-repressor or a kinase-inactive IKKbeta interferes with the neuroprotective activity of parkin. Furthermore, pathogenic parkin mutants with an impaired neuroprotective capacity show a reduced ability to stimulate NF-kappaB-dependent transcription. Finally, we present evidence that parkin interacts with and promotes degradation-independent ubiquitylation of IKKgamma/NEMO (NF-kappaB essential modifier) and TRAF2 [TNF (tumor necrosis factor) receptor-associated factor 2], two critical components of the NF-kappaB pathway. Thus, our results support a direct link between the neuroprotective activity of parkin and ubiquitin signaling in the IKK/NF-kappaB pathway.