http://purl.uniprot.org/citations/19682558 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/19682558 | http://www.w3.org/2000/01/rdf-schema#comment | "Pertussis toxin (PTX) treatment results in ADP-ribosylation of Gi-protein and thus in disruption of mu-opioid receptor signal transduction and loss of the antinociceptive effect of morphine. We have previously demonstrated that pretreatment with ultra-low dose naloxone preserves the antinociceptive effect of morphine in PTX-treated rats. The present study further examined the effect of ultra-low dose naloxone on mu-opioid receptor signaling in PTX-treated rats and the underlying mechanism. Male Wistar rats implanted with an intrathecal catheter received an intrathecal injection of saline or PTX (1 microg in 5 microl of saline), then, 4 days later, were pretreated by intrathecal injection with either saline or ultra-low dose naloxone (15 ng in 5 microl of saline), followed, 30 min later, by saline or morphine (10 microg in 5 microl of saline). Four days after PTX injection, thermal hyperalgesia was observed, together with increased coupling of excitatory Gs-protein to mu-opioid receptors in the spinal cord. Ultra-low dose naloxone pretreatment preserved the antinociceptive effect of morphine, and this effect was completely blocked by the mu-opioid receptor antagonist CTOP, but not by the kappa-opioid receptor antagonist nor-BNI or the delta-opioid receptor antagonist naltrindole. Moreover, a co-immunoprecipitation study showed that ultra-low dose naloxone restored mu-opioid receptor/Gi-protein coupling and inhibited the PTX-induced mu-opioid receptor/Gs-protein coupling. In addition to the anti-neuroinflammatory effect and glutamate transporter modulation previously observed in PTX-treated rats, the re-establishment of mu-opioid receptor Gi/Go-protein coupling is involved in the restoration of the antinociceptive effect of morphine by ultra-low dose naloxone pretreatment by normalizing the balance between the excitatory and inhibitory signaling pathways. These results show that ultra-low dose naloxone preserves the antinociceptive effect of morphine, suppresses spinal neuroinflammation, and reduces PTX-elevated excitatory Gs-coupled opioid receptors in PTX-treated rats. We suggest that ultra-low dose naloxone might be clinically valuable in pain management."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.neuroscience.2009.08.015"xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Wong C.S."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Tai Y.H."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Yeh C.C."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Tsai R.Y."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Cherng C.H."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/author | "Tzeng J.I."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/name | "Neuroscience"xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/pages | "435-443"xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/title | "Ultra-low dose naloxone restores the antinociceptive effect of morphine in pertussis toxin-treated rats by reversing the coupling of mu-opioid receptors from Gs-protein to coupling to Gi-protein."xsd:string |
http://purl.uniprot.org/citations/19682558 | http://purl.uniprot.org/core/volume | "164"xsd:string |
http://purl.uniprot.org/citations/19682558 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19682558 |
http://purl.uniprot.org/citations/19682558 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19682558 |
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