INT245587
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The difference in the neural wiring pattern such as the abundance of recurrent networks may underlie the different effects of NMDA receptor ablation in the hippocampal CA1 and CA3 regions on network activity. | |||||||||||||||
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Recording from the cortex and hippocampal CA1 region, spikes reversed their polarity in the CA1 stratum oriens. | |||||||||||||||
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In line of this criterion, we have indeed observed that these CA1 dynamics patterns reappeared at the time of both contextual and traced fear retention tests. | |||||||||||||||
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No staining was detected in the lacunosum-molecular layer in CA1, CA2 and CA3 (Figures 9b, 9c and 9d). | |||||||||||||||
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However, dissociations have also been shown; for example, in a fear conditioning task, it was shown, using oligonucleotide antisense, that regulation of the transcription factor, Zif268/Egr1 in CA1 of the hippocampus was not necessary for consolidating fear memory, but was necessary for reconsolidation of the active memory (Lee et al., 2004). | |||||||||||||||
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In contrast to the small, but significant, changes in average firing rates of putative pyramidal cells, the major effect of ketamine on CA1 was the dramatic change in ensemble dynamic patterns. | |||||||||||||||
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S1), subsequent neurogenesis actually partly restored the total neuron populations in the CA3 and CA1 regions. | |||||||||||||||
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In the hippocampal CA1 region where most of LTP studies have been reported, LTP can be induced and reliable detected, even with field recording electrodes [7,8]. | |||||||||||||||
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We then wondered whether these changes were specific to the SSC, and therefore evaluated the effects of these three anesthetics on the development of dendritic protrusions in another cortical region, area CA1 of the hippocampus, where cells also express YFP. | |||||||||||||||
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Similarly to observations made in the SSC, the effects of the three anesthetics on CA1 dendritic spines were dependent on the age of the animals (Fig. 4b), thus reproducing the changes observed in the SSC. | |||||||||||||||
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The number of Nissl-stained neuronal profile in areas CA3, CA1, the dentate hilus, and the dentate gyrus were counted in both the right and left hippocampus in horizontal sections for each animal by using four to five Nissl-stained sections that were ? | |||||||||||||||
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Infusion of activin A itself had no additional effect on astrocyte proliferation in the hippocampal DG, CA3, CA1, and pPV regions after KA injection (Fig. 3K). | |||||||||||||||
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To determine whether activin A had a role in this process, we first assessed whether activin A regulated the number of proliferating astrocytes in the DG, CA3, CA1, and pPV regions [7, 24]. | |||||||||||||||
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Mice were anaesthetized with tribromoethanol (200 mg/kg) and stereotaxic surgery was performed to implant a 3 mm cannula at -1.5 mm posterior and -2.0 mm lateral from bregma and 2.5 mm deep by the insertion of 2 spacers (0.25 mm each) to target the CA1 of the right hippocampus in each 2-month old C57BL/6 female mice [24]. | |||||||||||||||
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The changes in the CA1, CA2/3, and dentate gyrus were termed delayed neuronal death, reactive change, and ischemic cell change, respectively. | |||||||||||||||
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