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PMID:18042863

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Citation

Jones, TL, Lustig, AC and Sorkin, LS (2007) Secondary hyperalgesia in the postoperative pain model is dependent on spinal calcium/calmodulin-dependent protein kinase II alpha activation. Anesth. Analg. 105:1650-6, table of contents

Abstract

Spinally administered non-N-methyl-D-aspartate (NMDA), but not NMDA, receptor antagonists block primary (1 degree) and secondary (2 degrees) mechanical hyperalgesia and spontaneous pain after plantar incision. Hyperalgesia after thermal stimulation is also mediated by non-NMDA, but not NMDA, receptors. Although previous pain behavior studies in the thermal stimulus model demonstrated distinct protein kinase involvement downstream from spinal non-NMDA receptor activation, protein kinase signaling mechanisms have not been examined in the postoperative pain model. In the present study, we investigated whether spinal calcium/calmodulin-dependent protein kinase IIalpha (CaMKIIalpha) mediates 1 degree and/or 2 degrees hyperalgesia and spontaneous pain behavior after plantar incision.

Links

PubMed Online version:10.1213/01.ane.0000287644.00420.49

Keywords

Animals; Calcium-Calmodulin-Dependent Protein Kinase Type 2/genetics; Calcium-Calmodulin-Dependent Protein Kinase Type 2/metabolism; Disease Models, Animal; Enzyme Activation/physiology; Hyperalgesia/enzymology; Hyperalgesia/genetics; Male; Pain Measurement/methods; Pain, Postoperative/enzymology; Pain, Postoperative/genetics; Rats; Rats, Sprague-Dawley; Spinal Cord/enzymology

Significance

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Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

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