Neuroscience
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Recently, the empirical interest in religiousness and spirituality has grown, showing the association between the activity of a complex network of subcortical and fronto-parietal areas and explicit and implicit religious/spiritual representations. Importantly, while the causal link between parietal stimulation and implicit religiousness/spirituality has been demonstrated, the role of subcortical and medial cortical areas has not been directly investigated. Here, we assessed how implicit and explicit religious or spiritual representations are modulated by transcutaneous Vagus Nerve Stimulation (tVNS), a novel non-invasive method to stimulate subcortical and medial cortical structures. ⋯ Active-tVNS, compared to sham-tVNS, affected implicit spiritual, but not religious or control self-representations, reducing the strength of the automatic association between the self and the spiritual dimension. Explicit self-representations were left unchanged. Findings shed new light on the neurobiological mechanisms of implicit spirituality.
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Calpain-mediated tau cleavage into the neurotoxic tau45-230 fragment plays an important role in Alzheimer's disease (AD). This tau fragment accumulates mainly in the cytoplasm of degenerating neurons. However, subcellular localization studies indicated that a pool of tau45-230 associates with the cytoskeleton in hippocampal neurons. ⋯ The data obtained also showed a significant reduction in actin filaments in tau45-230-expressing neurons. These changes in microtubules and actin filaments correlated with delayed neurite elongation and axonal differentiation in the presence of this tau fragment. Together, these results suggest that tau45-230 could exert its toxic effects, at least in part, by modifying the composition of the neuronal cytoskeleton and impairing neurite elongation in neurons undergoing degeneration.
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Mesolimbic dopamine has been implicated in reward learning. Fischbach-Weiss and Janak (this issue) use optogenetics to attenuate dopamine signaling and study its role in cue-driven motivated behavior.
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Neuroinflammation is considered to be a critical component in the pathological process after intracerebral hemorrhage (ICH). Microglia are the foremost and earliest inflammatory cells participating in the pathological process of ICH. AdipoRon is the agonist of AdipoR1 (Adiponectin receptor 1), which enhances P-AMPK (phosphorylated AMP-activated protein kinase) activation. ⋯ The in vitro experiment showed that AdipoRon not only directly inhibited neuronal ROS overproduction, but also indirectly decreased the neuronal death in a transwell co-culture system. In summary, AdipoRon protects against ICH induced injury through promoting M2a microglia polarization and reducing neuronal death. These effects of AdipoRon rely on the activation of AdipoR1-AMPK signaling pathway.
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Reward-paired optogenetic manipulation of dopamine neurons can increase or decrease behavioral responding to antecedent cues when subjects have the opportunity for new learning, in accordance with a dopamine-mediated error learning signal. Here we examined the impact of reward-paired dopamine neuron inhibition on behavioral responding to reward-predictive cues after subjects had learned. We trained male TH-IRES-Cre mice to lever press for food reward in a progressive ratio procedure, a 2-cue choice procedure, or when continuously reinforced; in all procedures, completion of the response requirement was signaled by an auditory cue presented prior to food delivery. ⋯ Extinction-like behavioral responding was selective for learned associations: it was observed in the 2-cue choice procedure in which each subject was trained on two associations and inhibition was paired with reward for only one of the associations. Thus, inhibition during reward receipt can decrease responding to reward-predictive cues, sharing some features of behavioral extinction. These findings suggest changes in mesolimbic dopaminergic transmission at the time of experienced reward impacts subsequent responding to cues in well-trained subjects as predicted for a learning signal.