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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Premature or ill full-term infants are subject to a number of noxious procedures as part of their necessary medical care. Although we know that human infants show neural changes in response to such procedures, we know little of the sensory or affective brain circuitry activated by pain. In rodent models, the focus has been on spinal cord and, more recently, midbrain and medulla. ⋯ Formalin induced the oft-reported biphasic response at this age and induced a conditioned aversion to cues associated with its injection, thus demonstrating the aversiveness of the stimulation. Morphometric analyses, structural equation modeling and co-expression analysis showed that limbic and sensory paths were activated, the most prominent of which were the prefrontal and anterior cingulate cortices, nucleus accumbens, amygdala, hypothalamus, several brainstem structures, and the cerebellum. Therefore, both sensory and affective circuits, which are activated by pain in the adult, can also be activated by noxious stimulation in 12-day-old rat pups.
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The use of the existing endogenous neural progenitor cells (NPCs) in the brains of adult mammalian animals is challenging for cell therapy in treating Parkinson's disease (PD). Previous studies have indicated that there is a low level of neurogenesis in the substantia nigra (SN) of adult mice. To assess the regenerative/neurogenic capacity of NPCs following an intranigral injection of 6-hydroxydopamine (6-OHDA), the proliferation and differentiation of subventricular zone (SVZ)- and midbrain-derived NPCs were investigated, and the origin of SN newborn dopaminergic neurons was traced by using Nestin-CreER(TM)::ROSA26-LacZ mice and constructing a plasmid CD133-Promoter2-Cre. ⋯ The SN newly generated dopaminergic neurons might contribute a little to an incomplete recovery of the nigrostriatal system. In addition, we found that SN newborn dopaminergic neurons were mainly derived from the migration and differentiation of the NPCs in the 3V- and Aq-SVZ and their adjacent regions. Thus, it will become an ideal strategy to treat PD by promoting the proliferation and differentiation of endogenous NPCs.
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The Sonic hedgehog (Shh) signaling pathway is recapitulated in response to ischemic injury. Here, we investigated the clinical implications of Shh protein in the ischemic stroke and explored the underlying mechanism. Intracerebroventricular injection of Shh, Cyclopamine, or anti-vascular endothelial growth factor (VEGF) was performed immediately after permanent middle cerebral artery occlusion (pMCAO) surgery and lasted for 7days (d). ⋯ To observe in vitro angiogenesis, rat brain microvascular endothelial cells (RBMECs) were incubated under oxygen glucose deprivation (OGD) for 6h (h) and treated with Shh/anti-VEGF. We found that (1) Shh improved neurological scores and reduced infarct volume, which was blocked by Cyclopamine, (2) Shh improved the microvascular density and promoted angiogenesis and neuron survival in the ischemic boundary zone, (3) Shh enhanced VEGF expression and VEGF antibody could reverse angiogenic and protective effect of Shh in vivo and in vitro. These data demonstrate that the administration of Shh protein could protect brain from ischemic injury, in part by promoting angiogenic repair.
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Few minutes of focal vibration (FV) on limb muscles can improve motor control in neurological (stroke, Parkinson) patients for unknown underlying neurophysiological mechanisms. Here we hypothesized that in healthy volunteers this FV would increase excitability in the primary sensorimotor cortex (S1-M1) during an isometric contraction of the stimulated muscle. The design included an initial control condition with no FV stimulation (Baseline) as well as three short experimental sessions of FV and a Sham (fake) session in a pseudo-random order. ⋯ Results showed that, compared to the Baseline (no FV) or Sham stimulation, the first two FV sessions showed a cumulative increase in alpha (but not beta) MRPD at C3 electrode, suggesting a specific effect of vibration on the excitability of contralateral S1-M1 generating EEG "mu" rhythms. FV over limb muscles modulates neurophysiological oscillations enhancing excitability of contralateral S1-M1 in healthy volunteers. The proposed mechanism may explain the clinical effects of vibratory rehabilitation in neurological patients with motor deficits.