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Hosler, J.

Publications and source records attributed to Hosler, J..

3 recordsLinked to original sources

High-intensity cardiovascular exercise facilitates online motor skill learning, with no effect of BDNF genotype

Previous studies have demonstrated that exercise can influence motor skill learning. However, the specific components of learning primed by exercise remain unclear. This study examined the effect of a preceding bout of high intensity interval training (HIIT) on the acquisition of a novel motor skill. The investigation focused on whether improvement in skill across the session was attributable to online gains during active practice or offline rest periods between practice blocks. There was also exploration as to whether common polymorphisms of the BDNF and DRD2/ANKK1 genes that regulate plasticity, learning, and memory, influenced the relationship between exercise and motor learning. It was demonstrated that HIIT enhanced skill acquisition, but that the effects of HIIT priming were not specifically attributable to within-session online or offline learning processes. Contrary to research on overnight consolidation, there was no interaction between BDNF, nor DRD2/ANKK1 genotype, with exercise primed skill learning.

neuroscience↗

Pneumococcal H2O2 Reshapes Mitochondrial Function and Reprograms Host Cell Metabolism

Streptococcus pneumoniae (Spn), a primary cause of pneumonia, induces acute lung parenchymal damage through a unique metabolic pathway generating hydrogen peroxide (H2O2) as a byproduct. This study demonstrates that Spn-derived H2O2, primarily produced by pyruvate oxidase (SpxB), inhibits key tricarboxylic acid (TCA) cycle enzymes (aconitase, glutamate dehydrogenase, and -ketoglutarate dehydrogenase) in lung epithelial cells, leading to citrate accumulation and diminished NADH production for oxidative phosphorylation. RNA sequencing reveals SpxB-dependent upregulation of glycolytic genes (HIF1A, IER3, HK2, PFKP), restricting pyruvate entry into the TCA cycle and increasing glucose consumption and lactate/acetate production, indicative of a Warburg-like metabolic shift that may enhance bacterial survival. Notably, mitochondrial membrane potential remains largely preserved, with minimal apoptosis despite Spn-induced stress. These findings uncover a novel mechanism of Spn-driven host metabolic reprogramming, highlighting potential therapeutic targets for pneumococcal diseases. ImportanceStreptococcus pneumoniae remains a leading cause of community-acquired pneumonia worldwide, yet the mechanisms by which it manipulates host metabolism to promote its survival and pathogenesis are not fully understood. This study reveals a novel metabolic strategy whereby pneumococcus-derived hydrogen peroxide, generated by pyruvate oxidase (SpxB), disrupts the host TCA cycle and drives a Warburg-like metabolic shift in lung epithelial cells. By inhibiting key TCA cycle enzymes and rewiring glycolytic gene expression, S. pneumoniae effectively reprograms host cell metabolism to favor its persistence, while minimizing host cell apoptosis and maintaining mitochondrial function. These insights expand our understanding of host-pathogen metabolic interactions and identify potential metabolic vulnerabilities that could be targeted to mitigate tissue damage and improve treatment outcomes in pneumococcal pneumonia.

microbiology↗

Reinforcement Expectation in the Honey Bee (Apis mellifera): Downshifts in Reinforcement Show Conditioned Inhibition

When animals learn the association of a Conditioned Stimulus with an Unconditioned Stimulus, later presentation of the CS invokes a representation of the US. When the expected US fails to occur, theoretical accounts predict that conditioned inhibition can accrue to any other stimuli that are associated with this change in the US. Empirical work with mammals has confirmed the existence of conditioned inhibition. But the way it is manifested, the conditions that produce it, and determining whether it is the opposite of excitatory conditioning, are important considerations. Invertebrates can make valuable contributions to this literature because of the well-established conditioning protocols and access to the central nervous system for studying neural underpinnings of behavior. Nevertheless, while conditioned inhibition has been reported, it has yet to be thoroughly investigated in invertebrates. Here we evaluate the role of the unconditioned stimulus (US) in producing conditioned inhibition by using Proboscis Extension Response conditioning of the honey bee (Apis mellifera). Specifically, using variations of a feature-negative experimental design, we employ downshifts in US intensity relative to US intensity used during initial excitatory conditioning, to show that an odorant in an odor-odor mixture can become a conditioned inhibitor. We argue that some alternative interpretations to conditioned inhibition are unlikely. However, we show variation across individuals in how strongly they show Conditioned Inhibition, with some individuals possibly revealing a different means of learning about changes in reinforcement. We discuss how resolution of these differences is needed to fully understand whether and how Conditioned Inhibition is manifested in the honey bee, and whether it can be extended to investigate how it is encoded in the CNS. It is also important for extension to other insect models. In particular, work like this will be important as more is revealed of the complexity of the insect brain from connectome projects.

animal behavior and cognition↗