کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9428922 | 1297018 | 2005 | 5 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Pharmacological interactions between calcium/calmodulin-dependent kinase II α and TRPV1 receptors in rat trigeminal sensory neurons
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
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چکیده انگلیسی
Multiple lines of evidence suggest that calcium/calmodulin-dependent kinase II α (CaMKIIα) plays an important role in the spinal dorsal horn in nociceptive models of chemical, inflammatory and nerve injury. Moreover, CaMKIIα phosphorylates the vanilloid receptor type 1 (TRPV1), thereby regulating vanilloid agonist binding to the receptor. Herein, we have explored a possible interaction of CaMKIIα activity with the TRPV1 receptor in rat trigeminal ganglion (TG) neurons in vitro. Inhibition of CaMKIIα with KN-93 (5 μM) inhibited capsaicin (CAP)- and n-arachidonoyl-dopamine (NADA)-evoked calcitonin gene-related peptide (CGRP) release effectively decreasing the Emax for both compounds. This effect was not mimicked by the inactive compound KN-92 (5 μM), indicating that the effect was mediated by CaMKIIα inhibition. CAP also stimulated a significant â¼50% increase in autophosphorylation of CaMKIIα at Thr286/287. Immunocytochemistry for phospho-CaMKIIα indicated that this effect specifically occurred in TRPV1-positive TG neurons. These findings indicate that phopho-CaMKIIα is likely to play a role in presynaptic primary afferents in animal models of nociceptive hypersensitivity and provide support for CaMKIIα modulation of TRPV1 activity in sensory neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience Letters - Volume 389, Issue 2, 2 December 2005, Pages 94-98
Journal: Neuroscience Letters - Volume 389, Issue 2, 2 December 2005, Pages 94-98
نویسندگان
Theodore J. Price, Nathanial A. Jeske, Christopher M. Flores, Kenneth M. Hargreaves,