Proprioceptive neurons (PNs) are essential for the proper execution of all our movements by providing muscle sensory feedback to the central motor network. Here, using deep single cell RNAseq of ...adult PNs coupled with virus and genetic tracings, we molecularly identify three main types of PNs (Ia, Ib and II) and find that they segregate into eight distinct subgroups. Our data unveil a highly sophisticated organization of PNs into discrete sensory input channels with distinct spatial distribution, innervation patterns and molecular profiles. Altogether, these features contribute to finely regulate proprioception during complex motor behavior. Moreover, while Ib- and II-PN subtypes are specified around birth, Ia-PN subtypes diversify later in life along with increased motor activity. We also show Ia-PNs plasticity following exercise training, suggesting Ia-PNs are important players in adaptive proprioceptive function in adult mice.
Somatic sensation is defined by the existence of a diversity of primary sensory neurons with unique biological features and response profiles to external and internal stimuli. However, there is no ...coherent picture about how this diversity of cell states is transcriptionally generated. Here, we use deep single cell analysis to resolve fate splits and molecular biasing processes during sensory neurogenesis in mice. Our results identify a complex series of successive and specific transcriptional changes in post-mitotic neurons that delineate hierarchical regulatory states leading to the generation of the main sensory neuron classes. In addition, our analysis identifies previously undetected early gene modules expressed long before fate determination although being clearly associated with defined sensory subtypes. Overall, the early diversity of sensory neurons is generated through successive bi-potential intermediates in which synchronization of relevant gene modules and concurrent repression of competing fate programs precede cell fate stabilization and final commitment.
Since the delivery of sex education is not standardized across local and international secondary schools in Hong Kong, this study aims to assess and compare the knowledge level of sexually ...transmitted infections (STIs) between university students who attended local and international secondary schools in Hong Kong.
From January to March 2019, we conducted a cross-sectional survey among undergraduates at the University of Hong Kong. The primary outcome was STI knowledge as measured by a 29-item quiz. A higher quiz score meant a better STI knowledge level. Students' attitude toward sexual health and their sex education history was collected. Bivariate and multivariate analyses were conducted to evaluate the association factor with a better STI knowledge level.
Three hundred and ninety six students were included in the analysis. Three hundred thirty three (85.35%) students attended local secondary schools and 58 (14.65%) students attended international secondary schools in Hong Kong; 200 (50.51%) students were male and 196 (49.49%) students were female. Compared with students from local secondary school, those from international secondary schools had a significantly higher STI quiz score (18.19 vs. 15.4,
= 0.003). The results of multiple linear regression revealed that students in a higher year of study (β = 1.07,
< 0.001), from medical faculties (β = 6.96,
< 0.001), and from international secondary schools (β = 2.27,
= 0.003) achieved a higher STI quiz score.
University students who attended international secondary schools in Hong Kong possess a significantly higher knowledge level of STIs compared with those who attended local secondary schools. Nonetheless, the overall STI awareness among university students is inadequate. The inadequacy of STI awareness calls for the need to plan and implement satisfactory, comprehensive, and standardized sex education across the overall education system in Hong Kong.
Background
Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by the presence of tau tangles, amyloid beta plaques and neuroinflammation. Although the mechanisms ...underlying AD are not fully understand, several key risk factors for developing AD have been identified, such as depression. Previous work from our group, using a corticosterone‐induced model of depression in rats, has found that depression leads to tau phosphorylation and its displacement from microtubules, mislocalization and aggregation within neurons. The aims of my project are to continue investigating whether depression leads to other pathological tau alterations, such as acetylation, and to investigate the relationship between tau and neuroinflammation in the context of depression, focusing on the complement and toll‐like receptor (TLR) signaling pathways.
Method
In this project, we are using a corticosterone‐induced model of depression. Corticosterone is administered daily to Sprague‐Dawley (SD) rats for 21 days. Afterwards, a series of behavioral tests are performed including the Open Field test, the Novel Object Recognition task and the Forced Swim Test to assess their anxiety, memory and depressive behaviors, respectively. Afterwards, brain samples are collected from the animals to conduct immunohistochemical analysis, qPCR and western blot.
Result
Following 21 days of corticosterone administration, subjects display decreased adrenal and bodyweight, and anxiety‐like behaviors. Thus far, qPCR data demonstrates that there are increases in TLR4, as well as downstream elements in its signaling pathway, in the hippocampus.
Conclusion
In depression, alterations to the TLR4 signaling pathway are observed in the hippocampus. We will further investigate this pathway, its interplay with the complement system, and how these alterations impact tau pathology.
Abstract
Background
Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by the presence of tau tangles, amyloid beta plaques and neuroinflammation. Although the ...mechanisms underlying AD are not fully understand, several key risk factors for developing AD have been identified, such as depression. Previous work from our group, using a corticosterone‐induced model of depression in rats, has found that depression leads to tau phosphorylation and its displacement from microtubules, mislocalization and aggregation within neurons. The aims of my project are to continue investigating whether depression leads to other pathological tau alterations, such as acetylation, and to investigate the relationship between tau and neuroinflammation in the context of depression, focusing on the complement and toll‐like receptor (TLR) signaling pathways.
Method
In this project, we are using a corticosterone‐induced model of depression. Corticosterone is administered daily to Sprague‐Dawley (SD) rats for 21 days. Afterwards, a series of behavioral tests are performed including the Open Field test, the Novel Object Recognition task and the Forced Swim Test to assess their anxiety, memory and depressive behaviors, respectively. Afterwards, brain samples are collected from the animals to conduct immunohistochemical analysis, qPCR and western blot.
Result
Following 21 days of corticosterone administration, subjects display decreased adrenal and bodyweight, and anxiety‐like behaviors. Thus far, qPCR data demonstrates that there are increases in TLR4, as well as downstream elements in its signaling pathway, in the hippocampus.
Conclusion
In depression, alterations to the TLR4 signaling pathway are observed in the hippocampus. We will further investigate this pathway, its interplay with the complement system, and how these alterations impact tau pathology.
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