Neuroscience
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Our objective was to compare brain responses to trigeminal and olfactory stimuli in frequent and non-frequent gum chewers in order to explore whether habitual exposure to trigeminal stimuli affects their central-nervous processing. In healthy subjects, fMRI brain scans were obtained for 20 frequent gum chewers (GC) and 20 non-frequent gum chewers (N'GC), in response to four odorous stimuli; 2 'trigeminal' (peppermint and spearmint) and 2 non-trigeminal or 'olfactory' (cherry and strawberry). During measurements, subjects reported intensity and pleasantness ratings for all stimuli. ⋯ Apart from olfactory areas (amygdala, insular cortex), trigeminal odors also produced activations in right thalamus and right substantia nigra. (3) In the GC group, olfactory odors produced higher bilateral insular cortex activation than in N'GC group, but no such differences were observed for trigeminal odors. GC subjects appeared to be more responsive to trigeminal chemosensory stimuli. However, this did not directly translate into differences in central-nervous activations to trigeminal stimuli; instead, the use of chewing gum was associated with stronger brain activation towards olfactory stimuli.
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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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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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Protecting hippocampal neurons from death after seizure activity is critical to prevent an alteration of neuronal circuitry and hippocampal function. Here, we present a novel target, a truncated form of neogenin that is associated with seizure-induced hippocampal necroptosis, and novel use of the γ-secretase inhibitor N-[N-(3,5-difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester (DAPT) as a pharmacological regulator of neogenin truncation. We show that 3 days after pilocarpine-induced status epilepticus in mice, when hippocampal cell death is detected, the level of truncated neogenin is increased, while that of full-length neogenin is decreased. ⋯ In cultured hippocampal cells, kainic acid treatment significantly reduced the expression of full-length neogenin. Notably, treatment with DAPT prevented neogenin truncation and protected cultured neurons from N-methyl-D-aspartate (NMDA)-induced death. These data suggest that seizure-induced hippocampal necroptosis is associated with the generation of truncated neogenin, and that prevention of this by DAPT treatment can protect against NMDA-induced excitotoxicity.