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filingDate 2011-03-28-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_54b75fb6d1a4ceb94dc14baa4fad028b
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_b35768eb93b9a8b2876584607657a351
publicationDate 2011-07-21-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-2011178160-A1
titleOfInvention Inhibition of Interaction of PSD93 and PSDS95 with nNOS and NMDA Receptors
abstract PSD-95/SAP90 antisense-treated animals not only experience a significant decrease in MAC for isoflurane, but also experience an attenuation in the NMDA-induced increase in isoflurane MAC. PSD-95/SAP90 appears to mediate the role of the NMDA receptor in determining the MAC of inhalational anesthetics. Suppression of the expression of PSD-95/SAP90 in the spinal cord significantly attenuates responses to painful stimuli mediated through the N-methyl-D-aspartate receptor activation. In spinal cord neurons PSD-95/SAP90 interacts with the N-methyl-D-aspartate receptor subunits 2A/2B. Activation of the N-methyl-D-aspartate receptor in spinal hyperalgesia results in association of the N-methyl-D-aspartate receptor with PSD-95/SAP90. PSD-95/SAP90 is required for hyperalgesia triggered via the N-methyl-D-aspartate receptor at the spinal cord level.
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