Neuroscience
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Pain is a major health problem, affecting over fifty million adults in the US alone, with significant economic cost in medical care and lost productivity. Despite evidence implicating nicotinic acetylcholine receptors (nAChRs) in pathological pain, their specific contribution to pain processing in the spinal cord remains unclear given their presence in both neuronal and non-neuronal cell types. Here we investigated if loss of neuronal-specific TMEM35a (NACHO), a novel chaperone for functional expression of the homomeric α7 and assembly of the heteromeric α3, α4, and α6-containing nAChRs, modulates pain in mice. ⋯ These DEGs were mapped onto functional gene networks using the knowledge-based database, Ingenuity Pathway Analysis, and suggests increased neuroinflammation as a potential contributing factor for the hyperalgesia in tmem35a KO mice. Collectively, these findings implicate a heightened inflammatory response in the absence of neuronal NACHO activity. Additional studies are needed to determine the precise mechanism by which NACHO in the spinal cord modulates pain.
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It is known that the nucleus accumbens, orbitofrontal cortex and insula play a role in food-related reward processes. Although their interconnectedness would be an ideal topic for understanding food intake mechanisms, it nevertheless remains unclear especially in adolescent. Therefore, this study aims to investigate the effect of hunger on functional connectivity in healthy adolescents using task- and rest-based imaging. ⋯ Conversely, functional connectivity was increased during aversive stimuli between the right medial orbitofrontal cortex and right posterior insula when hungry as opposed to satiated. This suggests that the value of valence could occur in the shift in connectivity between these two regions. In addition, during rest-based imaging, a left-sided lateralization was reported (accumbens/lateral orbitofrontal and accumbens/posterior insula) when hungry as opposed to satiated which may represent changes in internal state due to focus on the benefit of an upcoming meal.
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During cultural transmission, caregivers typically adjust their form of speech according to the presumed characteristics of an infant/child, a phenomenon known as infant/child directed speech (IDS/CDS) or "parentese." Although ventromedial prefrontal cortex (vmPFC) damage was previously found to be associated with failure in adjusting non-verbal communicative behaviors, little is known about the neural mechanisms of verbal communicative adjustments, such as IDS/CDS. In the current study, 30 healthy mothers with preschool-age children underwent functional magnetic resonance imaging (fMRI) while performing a picture naming task which required them to name an object for either a child or an adult. In the picture naming task, mothers exhibited a longer naming duration in the toward-child condition than the toward-adult control condition. ⋯ These findings suggest that the vmPFC, which is included in the default mode network, is involved in optimizing communicative behaviors for the inter-generational transmission of knowledge. This function of the vmPFC may be considered as a prosocial drive to lead to prosocial communicative behaviors depending on the context. This study provides a better understanding of the neural mechanisms involved in communicative adjustments for children and insight into related applied research fields such as parenting, pedagogy, and education.
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Every year the Alzheimer's Association publishes a report that provides facts and figures indicating the public health, social and economic impact of Alzheimer's disease (AD). In addition, there are a number of reviews on the disease for general readers. Also, at congresses, AD is analyzed at different but not always related levels, leading to an "elephant as seen by blind men situation" for many of the participants. The review presented herein seeks to provide readers with a holistic view of how AD develops from various perspectives: the whole human organism, brain, circuits, neurons, cellular hallmarks, and molecular level.
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Nearly sixty years ago Fredrich Timm developed a histochemical technique that revealed a rich reserve of free zinc in distinct regions of the brain. Subsequent electron microscopy studies in Timm- stained brain tissue found that this "labile" pool of cellular zinc was highly concentrated at synaptic boutons, hinting a possible role for the metal in synaptic transmission. ⋯ Here, we delve into our current understanding of the many roles zinc plays in the brain, from influencing neurotransmission and sensory processing, to activating both pro-survival and pro-death neuronal signaling pathways. Moreover, we detail the many mechanisms that tightly regulate cellular zinc levels, including metal binding proteins and a large array of zinc transporters.