Neuroscience
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Phonological facilitation (PF) refers to a reduction of naming latencies when a phonologically related word is presented concurrently with the target picture, as compared to the presentation of phonologically unrelated words. According to spread of activation models of word production, this effect arises after lexical selection, during phonetic encoding, and is due to the co-activation of the phonemes shared by the target word and the distracter. Conversely, semantic interference (SI) is characterized by longer naming latencies when semantically related distracters are concurrently presented with the target picture. ⋯ In two experiments, we applied anodal transcranial direct current stimulation (tDCS) over the left superior temporal gyrus (LSTG) and left inferior frontal gyrus (LIFG) before a picture-word interference task in which auditory distracters, which could be phonologically related or unrelated, were presented at a SOA of 150ms or 300ms. While stimulating the LSTG significantly reduced the PF by decreasing RTs in phonologically unrelated trials, anodal tDCS over the LIFG did not affect PF. In line with previous results, our findings support the "activation by competition" model, pointing to inhibition between target and distracters nodes as the mechanism involved in the occurrence of PF and SI.
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Neonatal brain injury is a problem of global importance. To date, no causal therapies are available. A substance with considerable therapeutic potential is the endogenous neuropeptide secretoneurin (SN), which has proven to be beneficial in adult stroke. ⋯ SN has neuroprotective potential in neonatal brain injury. Its main action seems to be inhibition of apoptosis in the aftermath of the insult, predominantly in the hypoxic-only hemisphere. This might be explained by the less pronounced injury in this hemisphere, where blood flow and thus nutrient supply are maintained.
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The immune/inflammatory signaling molecule tumor necrosis factor α (TNFα) is an important mediator of both constitutive and plastic signaling in the brain. In particular, TNFα is implicated in physiological processes, including fever, energy balance, and autonomic function, known to involve the hypothalamic paraventricular nucleus (PVN). Many critical actions of TNFα are transduced by the TNFα type 1 receptor (TNFR1), whose activation has been shown to potently modulate classical neural signaling. ⋯ Dendritic profiles expressing TNFR1 were contacted by axon terminals, which formed non-synaptic appositions, as well as excitatory-type and inhibitory-type synaptic specializations. A smaller population of TNFR1-labeled axon terminals making non-synaptic appositions, and to a lesser extent synaptic contacts, with unlabeled dendrites was also identified. These findings indicate that TNFR1 is structurally positioned to modulate postsynaptic signaling in the PVN, suggesting a mechanism whereby TNFR1 activation contributes to cardiovascular and other autonomic functions.
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A number of studies have shown that sensory inputs from the hand can have a profound effect in stabilizing upright posture. This suggests that the central nervous system can extract information about body motion and external forces acting on the body from cutaneous sensory signals. ⋯ In this study we investigate whether this rapid change in activation of lower limb muscles is an invariant response determined by the pattern of somatosensory information arising from sensory receptors in the hand or whether it adapts to changes in postural stability. We manipulated lateral stability of upright stance by changing stance width which had no effect on the activation of upper limb muscles or hand kinematics, but produced profound changes in the activation patterns of lower limb muscles when perturbations were in the medial/lateral direction without affecting the activation patterns of muscles when perturbations were in the anterior/posterior direction.
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TRPV4 ion channels have a broad expression profile and were shown to contribute to enhanced pain sensation in inflammation. Directly blocking TRPV4 might run the risk of interfering with normal physiology, and has prompted to explore the interaction with the scaffolding protein AKAP79, an approach successfully used for TRPV1 channels. HEK293t cells express AKAP79, additional transfection did not sensitize human TRPV4. ⋯ A synthetic peptide, resembling these amino acids and extended by a positive region for transmembrane uptake, was tested. Sensitization of TRPV4 responses could be reduced after exposure to this 771-781::TAT peptide but not by a scrambled control peptide. This validates the concept of targeting the interaction between TRPV4 and AKAP79 and controlling increased TRPV4 activity.