INT198749
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Synaptophysin and PSD95 were downregulated in the hypothalamus and syntaxin 1a and synaptotagmin were significantly decreased in the cortex of Mecp2? | |||||||||||||||
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The rapid redistribution of PSD-95, and other PSD molecules, could cause rapid shifts in synapse size and strength towards the more active inputs.
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These measurements show that the retention time for PSD-95 and the size of the PSD-95 cluster are tightly coupled at the level of single synapses.
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These measurements show that the retention time for PSD-95 and the size of the PSD-95 cluster are tightly coupled at the level of single synapses.
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Both NR1 and PSD-95 were markedly reduced in the prefrontal cortex of HB-EGF KO mice (P<0.01 vs. control mice) (Fig. 4d, i, and j). | |||||||||||||||
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These knockout mice showed (a) behavioral abnormalities similar to those described in psychiatric disorders, which were ameliorated by typical or atypical antipsychotics, (b) altered dopamine and serotonin levels in the brain, (c) decreases in spine density in neurons of the prefrontal cortex, (d) reductions in the protein levels of the NR1 subunit of the N-methyl-D-aspartate (NMDA) receptor and post-synaptic protein-95 (PSD-95), (e) decreases in the EGF receptor, and in the calcium/calmodulin-dependent protein kinase II (CaMK II) signal cascade. | |||||||||||||||
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20HA co-immunoprecipitated with both NR1 and NR2B, even in the absence of PSD-95 (Figure 4A, lane 2 and 3, respectively). | |||||||||||||||
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These knockout mice showed (a) behavioral abnormalities similar to those described in psychiatric disorders, which were ameliorated by typical or atypical antipsychotics, (b) altered dopamine and serotonin levels in the brain, (c) decreases in spine density in neurons of the prefrontal cortex, (d) reductions in the protein levels of the NR1 subunit of the N-methyl-D-aspartate (NMDA) receptor and post-synaptic protein-95 (PSD-95), (e) decreases in the EGF receptor, and in the calcium/calmodulin-dependent protein kinase II (CaMK II) signal cascade. | |||||||||||||||
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General Comments
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