INT74815
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
In vivo antinociceptive activity of anti-rat mGluR1 and mGluR5 antibodies in rats. | |||||||||||||||
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In addition to comparing predicted ligand binding energies, we also investigated the details of the interactions between the ligand binding pockets and the ligands for mGluR5. | |||||||||||||||
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mGluR1, but not mGluR5, can account for the pain-related changes of excitatory and inhibitory transmission in CeLC neurons | |||||||||||||||
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The results obtained with highly selective antagonists for mGluR1 and mGluR5 [40,42,52,53] show that presynaptic mGluR1, but not postsynaptic mGluR5, can account for the pain-related changes of excitatory and inhibitory transmission in CeLC neurons. | |||||||||||||||
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It is known that NVmes neurons express mGluR5 receptors from birth [90], [91] and we have now shown that the annulospiral endings bind mGluR5 antibodies. | |||||||||||||||
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Compelling anatomical and electrophysiological studies have indicated the presence of mGluR1 and mGluR5 in the neuropil of all the trigeminal nuclei [15]. | |||||||||||||||
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In our experiments, the most important receptor in mediating astrocytic activation to sensory and CT inputs was mGluR5. | |||||||||||||||
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Finally, CaM binding to the mGluRs did not appear to be Ca2+-dependent. | |||||||||||||||
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To assess the role of Siah1a binding, specific group I mGluRs were heterologously expressed in sympathetic neurons from the rat superior cervical ganglion (SCG), which do not natively express mGluRs [37,38]. | |||||||||||||||
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Recent work has shown that Siah can bind group I metabotropic glutamate receptors (mGluRs), but the functional consequences of this interaction are unknown.
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Further studies will be needed to determine if group I mGluRs and Siah1a interact physiologically, and whether this interaction has functional consequences. | |||||||||||||||
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This interaction was specific for group I mGluRs, as it was not observed in the analogous sequences from group II (mGluR2) or group III (mGluR7) receptors. | |||||||||||||||
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General Comments
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