We here investigate whether the well-known laterality of spoken language to the dominant left hemisphere could be explained by the learning of sensorimotor links between a word's articulatory program and its corresponding sound structure. Human-specific asymmetry of acoustic-articulatory connectivity is evident structurally, at the neuroanatomical level, in the arcuate fascicle, which connects superior-temporal and frontal cortices and is more developed in the left hemisphere. Because these left-lateralised fronto-temporal fibres provide a substrate for auditory-motor associations, we hypothesised that learning of acoustic-articulatory coincidences produces laterality, whereas perceptual learning does not. Twenty subjects studied a large (n=48) set of novel meaningless syllable combinations, pseudowords, in a perceptual learning condition, where they carefully listened to repeatedly presented novel items, and, crucially, in an articulatory learning condition, where each item had to be repeated immediately, so that articulatory and auditory speech-evoked cortical activations coincided. In the 14 subjects who successfully passed the learning routine and could recognize the learnt items reliably, both perceptual and articulatory learning were found to lead to an increase of pseudoword-elicited event-related potentials (ERPs), thus reflecting the formation of new memory circuits. Importantly, after articulatory learning, pseudoword-elicited ERPs were more strongly left-lateralised than after perceptual learning. Source localisation confirmed that perceptual learning led to increased activation in superior-temporal cortex bilaterally, whereas items learnt in the articulatory condition activated bilateral superior-temporal auditory in combination with left-pre-central motor areas. These results support a new explanation of the laterality of spoken language based on the neuroanatomy of sensorimotor links and Hebbian learning principles.
Celebrity endorsement is omnipresent. However, despite its prevalence, it is unclear why celebrities are more persuasive than (equally attractive) non-famous endorsers. The present study investigates which processes underlie the effect of fame on product memory and purchase intention by the use of functional magnetic resonance imaging methods. We find an increase in activity in the medial orbitofrontal cortex (mOFC) underlying the processing of celebrity–product pairings. This finding suggests that the effectiveness of celebrities stems from a transfer of positive affect from celebrity to product. Additional neuroimaging results indicate that this positive affect is elicited by the spontaneous retrieval of explicit memories associated with the celebrity endorser. Also, we demonstrate that neither the activation of implicit memories of earlier exposures nor an increase in attentional processing is essential for a celebrity advertisement to be effective. By explaining the neural mechanism of fame, our results illustrate how neuroscience may contribute to a better understanding of consumer behavior.
Small nuclear and nucleolar RNAs (snRNAs and snoRNAs) are known to be functionally and evolutionarily conserved elements of transcript processing machinery. Here, we investigated the expression evolution of snRNAs and snoRNAs by measuring their abundance in the frontal cortex of humans, chimpanzees, rhesus monkeys, and mice. Although snRNA expression is largely conserved, 44% of the 185 measured snoRNA and 40% of the 134 snoRNA families showed significant expression divergence among species. The snRNA and snoRNA expression divergence included drastic changes unique to humans: A 10-fold elevated expression of U1snRNA and a 1,000-fold drop in expression ofSNORA29 The decreased expression of SNORA29 might be due to two mutations that affect secondary structure stability. Using in situ hybridization, we further localizedSNORA29expression to nucleolar regions of neuronal cells. Our study presents the first observation of snoRNA abundance changes specific to the human lineage and suggests a possible mechanism underlying these changes.
In December 2015, nearly 200 countries reached a historic agreement in Paris to limit greenhouse gas emissions in hopes of curbing global warming. Law360's Expert Analysis special series looks at the impact the agreement will have on policies in various regions and countries.
To gain success in the evolutionary “arms race”, venomous animals such as scorpions produce diverse neurotoxins selected to hit targets in the nervous system of prey. Scorpion α-toxins affect insect and/or mammalian voltage-gated sodium channels (Nav’s) and thereby modify the excitability of muscle and nerve cells. Although more than a hundred α-toxins are known and a number of them have been studied into detail, the molecular mechanism of their interaction with Nav’s is still poorly understood. Here, we employ extensive molecular dynamics simulations and spatial mapping of hydrophobic/hydrophilic properties distributed over the molecular surface of α-toxins. It is revealed that in spite of the small size and relatively rigid structure, these toxins possess modular organization from structural, functional and evolutionary perspectives. The more conserved and rigid “core module” is supplemented with the “specificity module” (SM) that is comparatively flexible and variable, and determines the taxon (mammal vs. insect) specificity of α-toxin activity. We further show that SMs in mammal toxins are more flexible and hydrophilic than in insect toxins. Concomitant sequence-based analysis of Nav’s extracellular loops suggests that α-toxins recognize the channels using both modules. We propose that the core module binds to the voltage-sensing domain of repeat IV, whereas the more versatile SM interacts with the pore domain in repeat I of Nav’s. These findings corroborate and expand the hypothesis on different functional epitopes of toxins that has been reported previously. In effect, we propose that the modular structure in toxins evolved to match the domain architecture of Nav’s.