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971.
《Journal of Physiology》2013,107(6):510-516
Prefrontal cortex (PFC) and posterior parietal cortex (PPC) are neural substrates for spatial cognition. We here review studies in which we tested the hypothesis that human frontoparietal cortex may function as a priority map. According to priority map theory, objects or locations in the visual world are represented by neural activity that is proportional to their attentional priority. Using functional magnetic resonance imaging (fMRI), we first identified topographic maps in PFC and PPC as candidate priority maps of space. We then measured fMRI activity in candidate priority maps during the delay periods of a covert attention task, a spatial working memory task, and a motor planning task to test whether the activity depended on the particular spatial cognition. Our hypothesis was that some, but not all, candidate priority maps in PFC and PPC would be agnostic with regard to what was being prioritized, in that their activity would reflect the location in space across tasks rather than a particular kind of spatial cognition (e.g., covert attention). To test whether patterns of delay period activity were interchangeable during the spatial cognitive tasks, we used multivariate classifiers. We found that decoders trained to predict the locations on one task (e.g., working memory) cross-predicted the locations on the other tasks (e.g., covert attention and motor planning) in superior precentral sulcus (sPCS) and in a region of intraparietal sulcus (IPS2), suggesting that these patterns of maintenance activity may be interchangeable across the tasks. Such properties make sPCS in frontal cortex and IPS2 in parietal cortex viable priority map candidates, and suggest that these areas may be the human homologs of the monkey frontal eye field (FEF) and lateral intraparietal area (LIP).  相似文献   
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973.
974.
《Cell》2021,184(19):5053-5069.e23
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975.
Guang Chen  Byungwoo Kang  Jack Lindsey  Shaul Druckmann  Nuo Li 《Cell》2021,184(14):3717-3730.e24
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976.
Summary The proliferation rate of differentiating fetal rat adrenocortical cells was studied in primary culture. In this system, stimulation with ACTH induces differentiation of zona glomerulosa-like cortical cells into zona fasciculata-like cells. Incorporation of bromodeoxyuridine (BrdU) was studied immunocytochemically by use of anti-BrdU antibody, and the proliferation rate was counted from the monolayer colonies of adrenocortical cells. After 21 days of cultivation in the absence of ACTH, the proliferation rate of zona glomerulosa-like cells was 10%. The rate slowly declined to 1% at the age of 100 days during continuous cultivation in the absence of ACTH. Stimulation with ACTH induced a strong inhibition in the proliferation rate (down to 2% during the first 24 h). Treatment with ACTH during the following 48 h led to an extremely intense proliferation of adrenocortical cells at a proliferation rate of 25%. Continuous treatment with ACTH up to 100 days led to a persistent growth of adrenocortical cells, and a proliferation rate over 2-fold higher than in control cells cultivated in the absence of ACTH. Thus, ACTH is the principal growth-promoting factor also in vitro, as has been found in in vivo studies. This growth effect is mediated by a biphasic course; at the beginning of differentiation the effect is inhibitory and is followed by a persistent stimulation of the growth of adrenocortical cells.  相似文献   
977.
利用Sprague—Dawley大鼠慢性肾盂积水,在不切开积水肾的前提下,直接观察活体肾皮质微循环。该方法无损伤,微循环观察效果好,为开展肾皮质微循环研究提供了一种新的方法。  相似文献   
978.
Available mounting media cause fading of histological preparations over time. A study was designed to find the most suitable medium for durable mounting of Araldite embedded semithin sections of rabbit cerebral cortex stained with toluidine blue and pyronin G. Among four synthetic mounting media tested, only DePeX prevented fading of the sections during the first month. All mounting media tested helped preserve staining intensity after one month, since the fading rate after one year is only about half that in sections prepared without mounting medium. The average optical density of sections after one year was higher in preparations mounted with DePeX than in sections treated with the other mounting techniques tested in this study. After one year, the average optical density of sections mounted with DePeX had decreased approximately 20%.  相似文献   
979.
980.
Abstract: The effects of chemical modification of a disulfide bond(s) (-SS-) or sulfhydryl group(s) (-SH) on the [3H]-flunitrazepam ([3H]FNZ) binding to membrane-bound or immunoprecipitated benzodiazepine (BZD) receptors (BZD-R) from bovine cerebral cortex were examined. Reduction of -SS- with dithiothreitol (DTT) brought about a reversible, time- and dose-dependent inhibition of [3H]FNZ binding to the membrane-bound BZD-R. Alkylation of the membranes with the -SH-modifying reagent iodoacetamide (IAA) or 5,5'-dithiobis-(2-nitrobenzoic acid) (DTNB) produced a slight inhibition of [3H]FNZ binding in a dose-dependent manner. Scatchard analysis of saturation curves of [3H]FNZ binding in the presence and absence of 5 m M DTT revealed changes in affinity without modification in the maximal binding capacity, thus indicating a competitive mode of interaction. DTT pretreatment of both the membrane-bound and the immunoprecipitated BZD-R led to [3H]FNZ binding inhibition. Consistent with the modification of a binding site is the observation that reduction of -SS- does not bear on the binding affinity, but rather reduces the number of sites. Complete protection from DTT inhibition of [3H]FNZ binding by FNZ (an agonist) or by Ro 15–1788 (an antagonist) suggests the presence of -SS- at, or very close to, the BZD recognition binding site. No protection against IAA or DTNB inhibition was provided by FNZ. Photoaffinity labeling experiments with [3H]FNZ revealed a clear-cut band of 50 kDa in native and alkylated membranes but an extremely weak label in 5 m M DTT/IAA-treated membranes. The present results provide evidence for the participation of a disulfide bond in the recognition binding site of the bovine cerebral cortex BZD-R.  相似文献   
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