Neuroscience
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In two experiments, we combined a semantic blocked naming paradigm with anodal transcranial direct current stimulation (tDCS) to shed light on the neural correlates of the semantic interference (SI) effect. In particular, prior to the naming task, anodal tDCS was applied over the left superior temporal gyrus (STG, Experiment 1) or the left inferior frontal gyrus (IFG, Experiment 2) to enhance cortical excitability in these regions. ⋯ Overall, our data confirm the existence of a distributed cortical network involved in lexical retrieval and show that both the left IFG and the left STG play a causal role in this process. In particular, the left IFG is likely to be critical in resolving the conflict between competitor lexical representations, while the left STG seems to be the neural locus of the lexical representational system, where competition among different lexical representations occurs.
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There is increasing evidence that alterations in the focus of attention result in changes in neural responding at the most peripheral levels of the auditory system. To date, however, those studies have not ruled out differences in task demands or overall arousal in explaining differences in responding across intermodal attentional conditions. The present study sought to compare changes in the response of cochlear outer hair cells, employing distortion product otoacoustic emissions (DPOAEs), under different, balanced conditions of intermodal attention. ⋯ Also consistent with our previous findings, DPOAE rapid adaptation, believed to be mediated by the medial olivocochlear efferents (MOC), was unaffected by changes in intermodal attention. The present findings indicate that manipulations in the conditions of attention, through the corticofugal pathway, and its last relay to cochlear outer hair cells (OHCs), the MOC, alter cochlear sensitivity to sound. These data also suggest that the MOC influence on OHC sensitivity is composed of two independent processes, one of which is under attentional control.
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In mice, microRNAs (miRNAs) are required for embryonic viability, and previous reports implicate miRNA participation in brain cortical neurogenesis. Here, we provide a more comprehensive analysis of miRNA involvement in cortical brain development. To accomplish this we used mice in which Dicer, the RNase III enzyme necessary for canonical miRNA biogenesis, is depleted from Nestin-expressing progenitors and progeny cells. ⋯ Doublecortin and Rnd2 were also increased and showed altered distribution, supporting a strong regulatory role for miRNAs in both early and late neuronal migration. In addition, GFAP staining at E15.5 was more intense and disorganized throughout the cortex with Dicer depletion. These results significantly extend earlier works, and emphasize the impact of miRNAs on neural progenitor cell proliferation, apoptosis, migration, and differentiation in the developing mammalian brain.
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Recently there has been a widespread interest in the development of kappa opioid receptor (KOPR) ligands for treatment of pain, depression and anxiety, and prevention of stress-induced drug relapse. However, most of these preclinical studies have been conducted using male experimental animals. In the present study we examined if sex differences exist in neural activity induced by the KOPR agonist trans-(±)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]-cyclohexyl) benzeneacetamide methanesulfonate (U50,488H). ⋯ In addition, we observed a notable sex difference in the basolateral amygdala; in males, U50,488H induced an increase in immuno-positive cell numbers but a decrease in females. However, across other brain regions males were generally more sensitive to U50,488H-induced alterations than females. These results suggest the need to include female subjects in studies examining emotional responses to KOPR ligands.
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Single prolonged stress (SPS) is a rodent model of post traumatic stress disorder that is comprised of serial application of restraint (r), forced swim (fs), and ether (eth) followed by a 7-day quiescent period. SPS induces extinction retention deficits and it is believed that these deficits are caused by the combined stressful effect of serial exposure to r, fs, and eth. However, this hypothesis remains untested. ⋯ Hippocampal and PFC GR expression was enhanced by SPS and most p-SPSs, however hippocampal GR expression was significantly larger following the full SPS exposure than all other conditions. Our findings suggest that the combined stressful effect of serial exposure to r, fs, and eth results in extinction retention deficits. The results also suggest that simple enhancements in GR expression in the hippocampus and PFC are insufficient to result in extinction retention deficits, but raise the possibility that a threshold-enhancement in hippocampal GR expression contributes to SPS-induced extinction retention deficits.