INT263683
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The membrane domains of NR2A and NR2B, however, are over 95% identical and are therefore unlikely to be responsible for the differential effect of loss of Neto1. | |||||||||||||||
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Altogether, the above findings establish that Neto1-null mice are impaired in hippocampal-dependent spatial learning. | |||||||||||||||
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The loss of Neto1, while having no effect on basal AMPAR-mediated synaptic transmission, suppresses LTP to a degree comparable to that observed in mice lacking NR2A [52] or its C-terminal tail [53]. | |||||||||||||||
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We have established that Neto1 is a critical component of the NMDAR complex, and that loss of Neto1 leads to impaired hippocampal LTP and hippocampal-dependent learning and memory. | |||||||||||||||
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The preferential effect of the loss of Neto1 on the abundance of synaptic, but not total, NR2A-containing NMDARs would not have been predicted from studies on the basis of the disruption of other NMDAR-interacting proteins. | |||||||||||||||
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Rather, loss of Neto1 and LEV-10 each leads to a reduction in synaptic localization of the cognate receptors, whereas loss of SOL-1 leads to a loss of function of normally distributed GLR-1. | |||||||||||||||
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Although Neto1 binds to both NR2A and NR2B, the loss of Neto1 leads to a reduction in the abundance of NR2A, but not NR2B, in the PSD fraction from hippocampus and a reduction in NR2A puncta in the CA1 region. | |||||||||||||||
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Removal of the cytoplasmic tail and transmembrane domain of Neto1 did not abolish the Neto1:NMDAR interaction (Figure 4B, lanes 2 and 3), suggesting that it was mediated by the ectodomain of Neto1. | |||||||||||||||
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To determine whether Neto1 is required for normal brain function in the mouse, we disrupted the Neto1 locus by homologous recombination in mouse embryonic stem (ES) cells. | |||||||||||||||
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