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This study elucidated the brain regions associated with the perception-driven suppression of mental imagery generation by comparing brain activation in a picture observation condition with that in a positive imagery generation condition. The assumption was that mental imagery generation would be suppressed in the former condition but not in the latter. The results show significant activation of the left posterior cingulate gyrus (PCgG) in the former condition compared to in the latter condition. This finding is generally consistent with a previous study showing that the left PCgG suppresses mental imagery generation. Furthermore, correlational analyses showed a significant correlation between the activation of the left PCgG and participants' subjective richness ratings, which are a measure of the clarity of a presented picture. Increased activity in the PCgG makes it more difficult to generate mental imagery. As visual perceptual processing and visual imagery generation are in competition, the suppression of mental imagery generation leads to enhanced visual perceptual processing. In other words, the greater the suppression of mental imagery, the clearer the presented pictures are perceived. The significant correlation found is consistent with this idea. The current results and previous studies suggest that the left PCgG plays a role in suppressing the generation of mental imagery.

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The present study attempts to locate brain regions that are related to vividness control, a hypothesized mechanism that reduces the vividness of negative imagery by controlling memory retrieval and emotion processing. The results showed that BOLD response in the left posterior cingulate gyrus in the negative imagery condition, in which activation of vividness control mechanisms was considered to be strong, was greater than that in the positive imagery condition, in which the activation of control mechanisms was considered to be weak. Moreover, the activation of this region negatively correlated with the subjective vividness of negative imagery. These results support the idea that the posterior cingulate gyrus may be involved in the suppression of imagery generation. Several previous studies have suggested that the posterior cingulate cortex is involved in both memory and emotion processing. Therefore, the current results indicate that the posterior cingulate gyrus may function as the vividness control mechanism.

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Since Aristotle, people have believed that metaphors and similes express the same type of figurative meaning, despite the fact that they are expressed with different sentence patterns. In contrast, recent psycholinguistic models have suggested that metaphors and similes may promote different comprehension processes. In this study, we investigated the neural substrates involved in the comprehension of metaphor and simile using functional magnetic resonance imaging (fMRI) to evaluate whether simile comprehension differs from metaphor comprehension or not. In the metaphor and simile sentence conditions, higher activation was seen in the left inferior frontal gyrus. This result suggests that the activation in both metaphor and simile conditions indicates similar patterns in the left frontal region. The results also suggest that similes elicit higher levels of activation in the medial frontal region which might be related to inference processes, whereas metaphors elicit more right-sided prefrontal activation which might be related to figurative language comprehension.

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Resting Ca(2+) absorption by cortical thick ascending limbs (CALs) is passive and proceeds through the paracellular pathway. In contrast, parathyroid hormone (PTH) stimulates active, transcellular Ca(2+) absorption (J(Ca)). The Ca(2+)-sensing receptor (CaSR) is expressed on serosal membranes of CALs. In the present study, we tested the hypothesis that activation of the CAL CaSR indirectly inhibits passive Ca(2+) transport and directly suppresses PTH-induced cellular J(Ca). To test this theory, we measured J(Ca) and Na absorption (J(Na)) by single perfused mouse CALs. Net absorption was measured microfluorimetrically in samples collected from tubules perfused and bathed in symmetrical HEPES-buffered solutions or those in which luminal Na(+) was reduced from 150 to 50 mM. We first confirmed that Gd(3+) activated the CaSR by measuring intracellular Ca(2+) concentration ([Ca(2+)](i)) in CALs loaded with fura 2. On stepwise addition of Gd(3+) to the bath, [Ca(2+)](i) increased, with a half-maximal rise at 30 microM Gd(3+). J(Ca) and transepithelial voltage (V(e),) were measured in symmetrical Na(+)-containing solutions. PTH increased J(Ca) by 100%, and 30 microM Gd(3+) inhibited this effect. V(e) was unchanged by either PTH or Gd(3+). Similarly, NPS R-467, an organic CaSR agonist, inhibited PTH-stimulated J(Ca) without altering V(e). Neither PTH nor Gd(3+) affected J(Na). Addition of bumetanide to the luminal perfusate abolished J(Na) and V(e). These results show that CaSR activation directly inhibited PTH-induced transcellular J(Ca) and that cellular Ca(2+) and Na(+) transport can be dissociated. To test the effect of CaSR activation on passive paracellular Ca(2+) transport, J(Ca) was measured under asymmetrical Na conditions, in which passive Ca(2+) transport dominates transepithelial absorption. PTH stimulated J(Ca) by 24% and was suppressed by Gd(3+). In this setting, Gd(3+) reduced V(e) by 32%, indicating that CaSR activation inhibited both transcellular and paracellular Ca(2+) transport. We conclude that the CaSR regulates both active transcellular and passive paracellular Ca(2+) reabsorption but has no effect on J(Na) by CALs.

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