Neuroscience
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A large number of studies have demonstrated costly punishment to unfair events across human societies. However, individuals exhibit a large heterogeneity in costly punishment decisions, whereas the neuropsychological substrates underlying the heterogeneity remain poorly understood. Here, we addressed this issue by applying a multivariate machine-learning approach to compare topological properties of resting-state brain networks as a potential neuromarker between individuals exhibiting different punishment propensities. ⋯ Importantly, the most discriminative features that contributed to the classification were those regions frequently implicated in costly punishment decisions, including dorsal anterior cingulate cortex (dACC) and putamen (salience network), dorsomedial prefrontal cortex (dmPFC) and temporoparietal junction (mentalizing network), and lateral prefrontal cortex (central-executive network). These networks are previously implicated in encoding norm violation and intentions of others and integrating this information for punishment decisions. Our findings thus demonstrated that resting-state functional connectivity (RSFC) provides a promising neuromarker of social preferences, and bolster the assertion that human costly punishment behaviors emerge from interactions among multiple neural systems.
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The human auditory change detection response known as mismatch negativity (MMN) is an auditory event-related potential that has been extensively used to investigate various aspects of human brain function and dysfunction. However, two competing views of the neural mechanism that underlie MMN have been a subject of debate for decades. The sensory memory hypothesis claims that the MMN reflects sensory memory-based change detection. ⋯ The paradigm expected that two successive MMNs would be elicited by the two successive acoustic deviations in the deviant tone pairs, but when the two tones composing the tone-pairs were close in frequency, the first MMN would be attenuated in amplitude due to lateral inhibition. The results demonstrate that only one (the second) MMN was observed when the two tones were close in frequency (330 Hz and 392 Hz), but two MMNs were observed when the two tones were distant in frequency (330 Hz and 3135 Hz). These results suggest that lateral inhibition is a neural mechanism that underlies the MMN response.
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Thiamine deficiency (TD) has been used as an experimental model in rodents to study the molecular mechanisms of neurodegeneration and its association with behavioral changes. The aims of the present study were to investigate the spatial cognitive performance of pyrithiamine-induced thiamine deficiency (PTD) in adult male rats and disclose the thalamic proteome alterations caused by a severe TD episode. After the onset of the neurological signs, such as seizure and/or loss of righting reflex, the TD treatment was interrupted. ⋯ These could explain the outcome in neurotransmitter release changes caused by TD, previously observed by our group and by other authors. These findings disclose the role of key proteins and metabolic pathways probably involved in the neurodegeneration process induced by TD. These proteins represent relevant molecular targets for future studies focusing also on the molecular basis of selective vulnerability of some brain areas to TD insult.
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Recent studies have demonstrated sexual dimorphisms in the mechanisms contributing to the development of chronic pain. Here we tested the hypothesis that microglia might preferentially regulate hyperalgesic priming in male mice. We based this hypothesis on evidence that microglia preferentially contribute to neuropathic pain in male mice via ionotropic purinergic receptor (P2XR) or p38 mitogen-activated protein kinase (p38) signaling. ⋯ Neither TNP-ATP nor skepinone could reverse priming once it had already been established in male mice suggesting that these pathways must be inhibited early in the development of hyperalgesic priming to have an effect. Our work is consistent with previous findings that P2XR and p38 inhibition can lead to male-specific effects on pain behaviors in mice. However, given that we did not observe microglial activation at time points where these drugs were effective, our work also questions whether these effects can be completely attributed to microglia.
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PACAP1-38, a ubiquitous and multifunctional regulator has been in the focus of neurotoxicity research due to its impressive neuroprotective potential. Although the literature extensively demonstrated its repressive effect on the apoptotic machinery in neurodegenerative models, there is a striking absence of analysis on its role in normal development. We performed quantitative analyses on caspase activity in developing retina upon 100, 50, 25 or 1 pmol intravitreal PACAP1-38 injection from postnatal day 1 (P1) through P7 in Wistar rats. ⋯ The fundamental novelty of these results is that PACAP1-38 induces apoptosis during early postnatal retinogenesis. The dose as well as stage-dependent response suggests that PACAP1-38 has a Janus face in apoptosis regulation. It not only inhibits development-related apoptosis, but as a long-term effect, facilitates it.