http://purl.uniprot.org/citations/20696160 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/20696160 | http://www.w3.org/2000/01/rdf-schema#comment | "Tuberoinfundibular peptide of 39 residues (TIP39) synthesizing neurons at the caudal border of the thalamus and in the lateral pons project to areas rich in its receptor, the parathyroid hormone 2 receptor (PTH2R). These areas include many involved in processing nociceptive information. Here we examined the potential role of TIP39 signaling in nociception using a PTH2R antagonist (HYWH) and mice with deletion of TIP39's coding sequence or PTH2R null mutation. Intracerebroventricular (icv) infusion of HYWH significantly inhibited nociceptive responses in tail-flick and hot-plate tests and attenuated the nociceptive response to hindpaw formalin injection. TIP39-KO and PTH2R-KO had increased response latency in the 55°C hot-plate test and reduced responses in the hindpaw formalin test. The tail-flick test was not affected in either KO line. Thermal hypoalgesia in KO mice was dose-dependently reversed by systemic administration of the cannabinoid receptor 1 (CB1) antagonist rimonabant, which did not affect nociception in wild-type (WT). Systemic administration of the cannabinoid agonist CP 55,940 did not affect nociception in KO mice at a dose effective in WT. WT mice administered HYWH icv, and both KOs, had significantly increased stress-induced analgesia (SIA). Rimonabant blocked the increased SIA in TIP39-KO, PTH2R-KO or after HYWH infusion. CB1 and FAAH mRNA were decreased and increased, respectively, in the basolateral amygdala of TIP39-KO mice. These data suggest that TIP39 signaling modulates nociception, very likely by inhibiting endocannabinoid circuitry at a supraspinal level. We infer a new central mechanism for endocannabinoid regulation, via TIP39 acting on the PTH2R in discrete brain regions."xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.expneurol.2010.08.004"xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/author | "Usdin T.B."xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/author | "Dimitrov E.L."xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/author | "Petrus E."xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/name | "Exp Neurol"xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/pages | "68-83"xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/title | "Tuberoinfundibular peptide of 39 residues (TIP39) signaling modulates acute and tonic nociception."xsd:string |
http://purl.uniprot.org/citations/20696160 | http://purl.uniprot.org/core/volume | "226"xsd:string |
http://purl.uniprot.org/citations/20696160 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20696160 |
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