kn-92 and Neuralgia

kn-92 has been researched along with Neuralgia* in 1 studies

Other Studies

1 other study(ies) available for kn-92 and Neuralgia

Article	Year
Ca(2+)/calmodulin-protein kinase IIalpha in the trigeminal subnucleus caudalis contributes to neuropathic pain following inferior alveolar nerve transection. Experimental neurology, 2005, Volume: 192, Issue:2 Calcium-calmodulin protein kinase IIalpha (CaMKIIalpha) is mainly found in brain cells, and the mRNA concentrates highly in the postsynaptic density. CaMKIIalpha is an effector of calcium and calmodulin mediated functions, and the phosphorylated CaMKIIalpha (pCaMKIIalpha) activates glutamate receptors, such as the AMPA receptor, and enhances its function. In the present study, we examined whether CaMKIIalpha in trigeminal brainstem neurons contributed to the neuropathic pain induced by inferior alveolar nerve (IAN) transection. Using immunohistochemistry and in situ hybridization, we found that the expression of CaMKIIalpha and pCaMKIIalpha increased in the trigeminal subnucleus caudalis (Vc) after IAN transection. The significant increase in the protein of CaMKIIalpha peaked at 30 min after IAN transection, and the mRNA of CaMKIIalpha increased from 2 to 14 days. Double immunofluorescent staining for CaMKIIalpha and MAP2, a marker of dendrite, revealed a significant increase in the overlapping area at 30 min after injury. This suggests that CaMKIIalpha protein is synthesized from the local mRNA pool in the dendrite 30 min after IAN transection and may quickly transmit information after nerve injury. In the behavioral test in which the escape threshold from mechanical stimulation to the lateral face was measured, intrathecal administration of KN-93, a CaMKII inhibitor, for 7 days significantly inhibited mechano-allodynia induced by IAN transection, as compared with administration of a control peptide. These data suggest that CaMKIIalpha in the trigeminal subnucleus caudalis may be involved in neuropathic pain caused by IAN transection. Topics: Animals; Behavior, Animal; Benzylamines; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Cell Count; Escape Reaction; Immunohistochemistry; In Situ Hybridization; Laminectomy; Male; Mandibular Nerve; Microtubule-Associated Proteins; Neuralgia; Pain Measurement; Physical Stimulation; Protein Kinase Inhibitors; Protein Serine-Threonine Kinases; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sulfonamides; Time Factors; Trigeminal Nuclei	2005

Article

Year

Ca(2+)/calmodulin-protein kinase IIalpha in the trigeminal subnucleus caudalis contributes to neuropathic pain following inferior alveolar nerve transection.

Experimental neurology, 2005, Volume: 192, Issue:2

Calcium-calmodulin protein kinase IIalpha (CaMKIIalpha) is mainly found in brain cells, and the mRNA concentrates highly in the postsynaptic density. CaMKIIalpha is an effector of calcium and calmodulin mediated functions, and the phosphorylated CaMKIIalpha (pCaMKIIalpha) activates glutamate receptors, such as the AMPA receptor, and enhances its function. In the present study, we examined whether CaMKIIalpha in trigeminal brainstem neurons contributed to the neuropathic pain induced by inferior alveolar nerve (IAN) transection. Using immunohistochemistry and in situ hybridization, we found that the expression of CaMKIIalpha and pCaMKIIalpha increased in the trigeminal subnucleus caudalis (Vc) after IAN transection. The significant increase in the protein of CaMKIIalpha peaked at 30 min after IAN transection, and the mRNA of CaMKIIalpha increased from 2 to 14 days. Double immunofluorescent staining for CaMKIIalpha and MAP2, a marker of dendrite, revealed a significant increase in the overlapping area at 30 min after injury. This suggests that CaMKIIalpha protein is synthesized from the local mRNA pool in the dendrite 30 min after IAN transection and may quickly transmit information after nerve injury. In the behavioral test in which the escape threshold from mechanical stimulation to the lateral face was measured, intrathecal administration of KN-93, a CaMKII inhibitor, for 7 days significantly inhibited mechano-allodynia induced by IAN transection, as compared with administration of a control peptide. These data suggest that CaMKIIalpha in the trigeminal subnucleus caudalis may be involved in neuropathic pain caused by IAN transection.

Topics: Animals; Behavior, Animal; Benzylamines; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Cell Count; Escape Reaction; Immunohistochemistry; In Situ Hybridization; Laminectomy; Male; Mandibular Nerve; Microtubule-Associated Proteins; Neuralgia; Pain Measurement; Physical Stimulation; Protein Kinase Inhibitors; Protein Serine-Threonine Kinases; Rats; Rats, Sprague-Dawley; RNA, Messenger; Sulfonamides; Time Factors; Trigeminal Nuclei

2005