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Simoes, M.

Publications and source records attributed to Simoes, M..

3 recordsLinked to original sources

The cortical heartbeat-evoked potential is modulated by heart rate in a task and mental effort dependent manner

Cardiac cycle duration, or interbeat interval (IBI), is the period from one heartbeat to the next. IBI changes from cycle to cycle. Periods with longer IBI are associated with higher sensitivity to external sensory stimuli (exteroception). Warning cues induce a state of attentive anticipation characterized by an increase in IBI (anticipatory cardiac deceleration) and faster reaction times. Ageing reduces the increase in IBI induced by warning cues and response speed. However, it is unclear which mechanism, if any, connects IBI with reaction time. The heartbeat-evoked potential (HEP) is a cortical response evoked by the heartbeat, modulated by attention and associated with sensitivity to external sensory stimuli. HEP might be affected by IBI and mediate the association between cardiac output and cortical processing. We investigated if the HEP was affected by warning cues as well as spontaneous fluctuations in IBI. To explore the impact of age-related changes in cardiac responses, we included young and older people [N = 33/29; 26/23 women; mean age 23/61 years]. We analysed the electroencephalograms and electrocardiograms simultaneously acquired during auditory cued simple reaction time and go/no-go tasks. The warning cue did not induce significant changes in the HEP. Yet, fluctuations in IBI (not locked with the warning cue) affected the HEP and HEP amplitude was associated with average reaction time in the older group. However, on a trial-by-trial basis, reaction time was independent from IBI fluctuations. In conclusion, we found no evidence that the HEP mediates the effect of attention orienting on reaction time.

neuroscience↗

Morphine alleviates pain after heart cryoinjury in zebrafish without impeding regeneration

Nociceptive response belongs to a basic animal behavior facilitating adaptability and survival upon external or internal stimuli. Fish, similarly to higher vertebrates, also possess nociceptive machinery. Current protocols involving procedures performed on adult zebrafish including heart cryoinjury do not, however, take into account the adverse effects including pain that may potentially arise from these methodologies. Here, we assess the effect of two analgesics, lidocaine and morphine, followed after heart cryoinjury in zebrafish. Monitoring swimming behavior together with histology and gene expression analysis at the single cell level using scRNA sequencing and RNAscope fluorescent in situ hybridization technology, we show morphine, but not lidocaine, significantly improves animal welfare 6 hours post-cryoinjury, without impairing the heart regeneration process. Altogether, we propose morphine to be considered as the analgesic of choice to reduce post-surgical pain in adult zebrafish. HighlightsO_LICryoinury could be considered as a potential noxious stimulus in adult zebrafish. C_LIO_LIMorphine but not lidocaine treatment effectively alleviates noxious effects post-cryoinjury. C_LIO_LILidocaine treatment delays heart repair and regeneration. C_LIO_LI6 hours Morphine treatment after cryoinjury does not impede heart regeneration. C_LI

developmental biology↗

CD300lf is the primary physiologic receptor of murine norovirus but not human norovirus

Murine norovirus (MNoV) is an important model of human norovirus (HNoV) and mucosal virus infection more broadly. Viral receptor utilization is a major determinant of cell tropism, host range, and pathogenesis. The bona fide receptor for HNoV is unknown. Recently, we identified CD300lf as a proteinaceous receptor for MNoV. Interestingly, its paralogue CD300ld was also sufficient for MNoV infection in vitro. Here we explored whether CD300lf is the sole physiologic receptor in vivo and whether HNoV can use a CD300 ortholog as an entry receptor. We report that both CD300ld and CD300lf are sufficient for infection by diverse MNoV strains in vitro. We further demonstrate that CD300lf is essential for both oral and parenteral MNoV infection and to elicit anti-MNoV humoral responses in vivo. In mice deficient in STAT1 signaling, CD300lf is required for MNoV-induced lethality. However, after high dose intraperitoneal challenge with MNoV in Cd300lf-/-Stat1-/- mice a single amino acid mutation in the MNoV capsid protein emerged. This substitution did not alter receptor utilization in vitro. Finally, we demonstrate that human CD300lf (huCD300lf) is not essential for HNoV infection, nor does huCD300lf inhibit binding of HNoV virus-like particles to glycans. Thus, we report huCD300lf is not a receptor for HNoV. Author SummaryHuman norovirus is the leading cause of non-bacterial gastroenteritis causing up to 200,000 deaths each year. How human norovirus enters cells is unknown. Because human norovirus is difficult to grow in the laboratory and in small animals, we use mouse or murine norovirus as a model system. We recently discovered that murine norovirus can use the either CD300ld or CD300lf as a receptor in vitro. We also showed that CD300lf deficient mice were resistant to oral challenge with a single virus strain. Here we determined that CD300lf is essential for infection of diverse murine norovirus strains in cell lines and in mice with normal immune systems demonstrating its the primary physiologic receptor for diverse murine norovirus strains independent of infection route. However, in immunodeficient mice injected with high dose virus directly into the abdominal cavity, we observed a norovirus mutant that enabled CD300lf-independent infection. Finally, we demonstrated that human CD300lf is not the elusive receptor for human norovirus.

microbiology↗