Neuroscience
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As we move through our environment, our visual system is presented with optic flow, a potentially important cue for perception, navigation and postural control. How does the brain anticipate the optic flow that arises as a consequence of our own movement? Converging evidence suggests that stimuli are processed differently by the brain if occurring as a consequence of self-initiated actions, compared to when externally generated. However, this has mainly been demonstrated with auditory stimuli. ⋯ Furthermore, participants' visual induced motion sickness (VIMS) and vection intensity ratings correlated positively across the group - although many participants felt vection in the absence of any VIMS, none reported the opposite combination. Finally, we found that the simple act of making a button press leads to a detectable head movement even when using a chin rest. Taken together, our results indicate that the visual system is capable of predicting optic flow when self-initiated, to affect behaviour.
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Optic neuropathies comprise a group of disorders in which the axons of retinal ganglion cells (RGCs), the retinal projection neurons conveying visual information to the brain, are damaged. This results in visual impairment or even blindness, which is irreversible as adult mammals lack the capacity to repair or replace injured or lost neurons. Despite intensive research, no efficient treatment to induce axonal regeneration in the central nervous system (CNS) is available yet. ⋯ Interestingly, the pattern of the autophagic response in the axons followed the spatiotemporal window of axonal regrowth, which suggests that autophagy is ongoing at the growth cones. Pharmacological inhibition of the recycling pathway resulted in accelerated RGC target reinnervation, possibly linked to increased mechanistic target of rapamycin (mTOR) activity, known to stimulate axonal regrowth. Taken together, these intriguing findings underline that further research is warranted to decipher if modulation of autophagy could be an effective therapeutic method to induce CNS regeneration.
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Despite the growing emphasis on embedding interactive social paradigms in the field of cognitive and affective neuroscience, the impact of socially induced emotions on cognition remains widely unknown. The aim of the present study was to fill this gap by testing whether facial stimuli whose emotional valence was acquired through social learning in an economic trust game may influence cognitive performance in a subsequent stop-signal task. The study was designed as a conceptual replication of previous event-related potential experiments, extending them to more naturalistic settings. ⋯ The results revealed that the trust game was an effective paradigm for the induction of differently valenced emotions towards players; however, behavioral inhibitory performance was comparable in all stop-signal conditions. On the neural level, we found decreased P3 amplitude in negative trials due to significantly stronger activation in the right frontoparietal control network, which is involved in theory-of-mind operations and underlies social abilities in humans, especially memory-guided inference of others' mental states. Our findings make an important contribution to the cognition-emotion literature by showing that social interactions that take place during an economic game may influence brain activity within the mentalizing network in a subsequent cognitive task.
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Elevation of CSF Sortilin Following Subarachnoid Hemorrhage in Patients and Experimental Model Rats.
Subarachnoid hemorrhage (SAH) can cause acute neuronal injury and chronic neurocognitive deficits; biomarkers reflecting its associated neuronal injury are of potential prognostic value. Sortilin, a member of the vacuolar protein sorting 10p (Vps10p) family, is enriched in neurons and is likely involved in neurodegenerative diseases. Here, we explored sortilin in the cerebrospinal fluid (CSF) as a potential biomarker for early neuronal injury after SAH. ⋯ In immunohistochemistry, the pattern of sortilin labeling in the brain was largely comparable between the SAH and control rats, whereas an increased astrocytic GFAP immunolabeling was evident in the former. Together, these results suggest that SAH can cause an early and remarkable rise of sortilin products in CSF, likely reflecting neuronal change. Sortilin could be further explored as a potential biomarker in some brain disorders.