Neuroscience
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Sensitivity and reliability of animal behavioral assessment methods are critical for successful translation of in vitro findings to in vivo. Here we report a data transformation process in the elevated open platform task that generates a novel parameter, namely peak tolerance of fear (PTF) or its inversely correlated equivalent of anxiety quotient (AQ), to measure anxiogenic tendency in rodent. As compared to traditional parameters such as travel distance, time, or entries, PTF or AQ displays largely reduced data dispersion not only ingroup but also cross-study and cross-cohort, therefore representing a significant improvement of the methodology for rodent anxiety assessment.
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Difficulty understanding speech-in-noise (SIN) is a pervasive problem faced by older adults particularly those with hearing loss. Previous studies have identified structural and functional changes in the brain that contribute to older adults' speech perception difficulties. Yet, many of these studies use neuroimaging techniques that evaluate only gross activation in isolated brain regions. ⋯ Additionally, we found top-down β connectivity between prefrontal and auditory cortices strengthened with poorer hearing thresholds despite minimal behavioral differences. This is consistent with the proposal that linguistic brain areas may be recruited to compensate for impoverished auditory inputs through increased top-down predictions to assist SIN perception. Overall, these results emphasize the importance of top-down signaling in low-frequency brain rhythms that help compensate for hearing-related declines and facilitate efficient SIN processing.
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This study aims to investigate topological organization of cortical thickness and functional networks by cortical lobes. First, I demonstrated modular organization of these networks by the cortical surface frontal, temporal, parietal and occipital divisions. Secondly, I mapped the overlapping edges of cortical thickness and functional networks for positive and negative correlations. Finally, I showed that overlapping positive edges map onto within-lobe cortical interactions and negative onto between-lobes interactions.
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Synaptosomal-associated protein 25 (SNAP-25) plays an important role in neuropathic pain. However, the underlying mechanism is largely unknown. Vesicular glutamate transporter 2 (VGluT2) is an isoform of vesicular glutamate transporters that controls the storage and release of glutamate. ⋯ In pheochromocytoma (PC12) cells, the expression of VGluT2 was also depended on SNAP-25 dysregulation. Moreover, we found VGluT2 was involved in SNAP-25-mediated regulation of astrocyte expression and activation of the PKA/p-CREB pathway mediated the upregulation of SNAP-25 in neuropathic pain. The findings of our study indicate that VGluT2 contributes to the effect of SNAP-25 in maintaining the development of neuropathic pain and suggests a novel mechanism underlying SNAP-25 regulation of neuropathic pain.
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Despite the long history of investigations of adrenergic compounds and their biological effects, specific mechanisms of their action in distinct compartments of the motor unit remain obscure. Recent results have suggested that not only skeletal muscles but also the neuromuscular junctions represent important targets for the action of catecholamines. In this paper, we describe the effects of adrenaline and noradrenaline on the frequency of miniature endplate potentials, the quantal content of the evoked endplate potentials and the kinetics of acetylcholine quantal release in the motor nerve endings of the mouse diaphragm. ⋯ Quantal release became more asynchronous under noradrenaline, as evidenced by a greater dispersion of real synaptic delays; in contrast, adrenaline synchronized the release process. Our data suggest an involvement of α and β adrenoreceptors in the diverse modulation of the frequency of miniature endplate potentials, the quantal content of the evoked endplate potentials and the kinetics of acetylcholine quantal secretion in the mouse neuromuscular junction. Moreover, the adrenoblockers affected both the evoked and spontaneous quantal release of acetylcholine, suggesting the presence of endogenous catecholamines in the vicinity of cholinergic synapses.