Neuroscience
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As we listen to everyday sounds, auditory perception is heavily shaped by interactions between acoustic attributes such as pitch, timbre and intensity; though it is not clear how such interactions affect judgments of acoustic salience in dynamic soundscapes. Salience perception is believed to rely on an internal brain model that tracks the evolution of acoustic characteristics of a scene and flags events that do not fit this model as salient. The current study explores how the interdependency between attributes of dynamic scenes affects the neural representation of this internal model and shapes encoding of salient events. ⋯ Salient notes embedded in these scenes deviate from the melody's statistical distribution along pitch, timbre and/or intensity. Recordings of brain responses to salient notes reveal that neural power in response to the melodic rhythm as well as cross-trial phase alignment in the theta band are modulated by degree of salience of the notes, estimated across all acoustic attributes given their probabilistic context. These neural nonlinear effects across attributes strongly parallel behavioral nonlinear interactions observed in perceptual judgments of auditory salience using similar dynamic melodies; suggesting a neural underpinning of nonlinear interactions that underlie salience perception.
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The interconnectivity between brain development and the immune system has become an area of interest for many neuroscientists. However, to date, a limited number of known immune mediators of the peripheral nervous system (PNS) have been found to influence the development of the central nervous system (CNS). FOXP3 is a well-established mediator of regulatory T-cells in the PNS. ⋯ In the PNS, Foxp3 protein levels were low embryonically and increased steadily over the life of the animal with maximal levels reached in adulthood. Patterns observed for both the PNS and CNS were similar in males and females across all developmental timepoints. Our novel findings have implications for understanding how the neural immune system impacts neurodevelopmental disorders such as autism and schizophrenia.
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Previous studies have shown that aging is associated with changes in decision behavior. However, the neural mechanisms that underpin such age differences are inadequately understood. In this study, we aim to characterize the optimal neural model underlying a dynamic decision making task in both young and older adults, and further examine the age differences from the perspective of effective connectivity. ⋯ The dynamic causal modeling analysis, with the coupling between the ventromedial prefrontal cortex (VMPFC), dorsolateral prefrontal cortex (DLPFC) and anterior insula (AI) that were identified in our task-related activation and psychophysiological interaction analysis, was performed to address the best fitting neural model and characterize age differences. Although both age groups adopted the same optimal model with bidirectional connection between the VMPFC and DLPFC, older adults exhibited up-regulation in several connections and among which the increased modulatory effect of AI-to-VMPFC subserving their decision quality. Our finding suggests that older adults might utilize different neural strategy via compensation to counteract the impact of advanced age in risk taking process.
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Recent genome-wide association studies (GWAS) have found cerebellum as a top hit for sleep regulation. Restless legs syndrome (RLS) is a sleep-related sensorimotor disorder characterized by uncomfortable sensations in the extremities, generally at night, which are often relieved by movements. Clinical studies have found that RLS patients have structural and functional abnormalities in the cerebellum. ⋯ Btbd9 pKO mice also had an increased probability of waking at rest. Unlike the Btbd9 knockout mice, there was no increased thermal sensation in the Btbd9 pKO. Our results indicate that the Btbd9 knockout influences the PC activity; dysfunction in the cerebellum may contribute to the motor restlessness found in the Btbd9 knockout mice.
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α-Synuclein (α-Syn) is a key pathogenic protein in α-synucleinopathies including Parkinson disease (PD) and Dementia with Lewy Bodies. The aggregation of α-Syn is believed to be deleterious and a critical step leading to neuronal dysfunction and death. One of the factors that may contribute to the initial steps of this aggregation is crosslinking through transglutaminase 2 (TG2). ⋯ These neuropathological markers of diminished α-Syn toxicity in the absence of TG2 were associated with better motor performance on the rotarod and balance beam. These results suggest that deleting TG2 reduces the toxicity of α-Syn in vivo and improves the behavioral performance of SynTg mice. Accordingly, these findings collectively support pharmacological inhibition of TG2 as a potential disease modifying therapeutic strategy for α-synucleinopathies.