INT97099
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
As the majority of PSD-95:GFP puncta were typically juxtaposed against functional presynaptic boutons (Figure S1; see also [35]), the observed increases in PSD-95:GFP puncta number reflected, in all likelihood, increased numbers of glutamatergic synapses. | |||||||||||||||
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An interesting finding was the observation that high levels of network activity were associated with gradual increases in PSD-95:GFP puncta numbers, whereas suppressed activity levels were associated with gradual decreases in PSD-95:GFP puncta numbers (see also [82],[83]). | |||||||||||||||
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Our previous work has shown that PSD-95/SAP90 is required for NMDA receptor-mediated thermal hyperalgesia. | |||||||||||||||
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CONCLUSION: The results indicate not only a significant decrease in MAC for isoflurane but also an attenuation in the NMDA-induced increase in isoflurane MAC in the PSD-95/SAP90 antisense-treated animals, which suggests that PSD-95/SAP90 may mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics.
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To determine whether the observed changes in PSD-95:GFP puncta number and fluorescence intensity were dependent on changes in network activity, we repeated the experiments described above except that here, spontaneous network activity was blocked by adding tetrodotoxin (TTX) about an hour after the experiments were started. | |||||||||||||||
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In practically all experiments, we observed a gradual increase in the total number of PSD-95:GFP puncta, mainly (but not exclusively) due to increased density of PSD-95:GFP puncta along existing dendritic segments, at both spine tips and shafts (Figures 1C and 3B). | |||||||||||||||
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Our findings that suppression of activity broadens the distribution of PSD-95:GFP puncta fluorescence intensities and increases mean PSD-95:GFP fluorescence (Figures 3 and 5) are in general agreement with the aforementioned studies (see also [77],[82]). | |||||||||||||||
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Fluoxetine produced a small but significant increase in hippocampal PSD-95 in ovariectomized wildtype mice but not in ovariectomized TrkB.T1 mice or sham mice. | |||||||||||||||
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Specifically, GABA-A alpha1 subunit, GRIA1 subunit and PSD-95 mRNAs were decreased in the shell but increased in the core following morphine administration. | |||||||||||||||
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In the core, neuronal apoptotic inhibitory protein (NAIP), GABA-A alpha1 subunit, GRIN2C, GRIA1, mGluR1, D4 dopamine receptor and PSD-95 were upregulated by morphine administration whereas bax, bcl-x, cox-1 and MAP2 were decreased. | |||||||||||||||
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When compared with a baseline reflex activity with a single action potential evoked by the TS before the administration of test agents, MO instillation into the descending colon sensitized the evoked activity characterized by elongated firing in the reflex activity in association with increased protein levels of Cdk5, PSD95, and phosphorylated NR2B (pNR2B) but not of total NR2B (tNR2B) in the spinal cord tissue. | |||||||||||||||
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Comparison of gene expression between the shell and core subregions of vehicle-treated rats revealed significantly higher relative abundance of GABA-A alpha1, Galphai2 and post-synaptic density protein 95 transcript (PSD-95) mRNA levels in the shell, whereas Ggamma2 and synuclein 1 were more abundant in the core of the NAc. | |||||||||||||||
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Our previous work has shown that PSD-95/SAP90 is required for NMDA receptor-mediated thermal hyperalgesia. | |||||||||||||||
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CONCLUSION: The results indicate not only a significant decrease in MAC for isoflurane but also an attenuation in the NMDA-induced increase in isoflurane MAC in the PSD-95/SAP90 antisense-treated animals, which suggests that PSD-95/SAP90 may mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics.
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Expression of behavioral sensitization in RHA-I rats activated secretogranin and PSD-95 mRNA in the nucleus accumbens core. | |||||||||||||||
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The interactions with these synaptogenic factors suggest a potential role of PSD-95 and CASK in synapse formation. | |||||||||||||||
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Ca2+ acts as a cosignal with PSD-95, a postsynaptic density protein for activation of neuronal NOS and thus couples NMDA receptor activation to NO, which, in excess, is toxic to RGCs [149]. | |||||||||||||||
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General Comments
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