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نسخه‌ی کامل: converse white
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Results: The method elicited intermittent, head-directed wiping and scratching as well as the expression of both the c-FOS gene in the spinal trigeminal nucleus caudalis and calcitonin gene related peptide (CGRP) in the periaqueductal grey matter. Interestingly, the acid-induced trigeminal pain behaviour was inhibited by amiloride, an antagonist converse black of acid-sensing ion channels (ASICs), but not by AMG-9810, an inhibitor of transient receptor potential cation channel V1(TRPV1). In addition, the relative mRNA and protein expression levels of ASIC1a and ASIC3 were increased in the acid-induced trigeminal nociceptive pathways.

Acidic solutions have been shown to activate both ASICs and converse high tops TRPV1 [ 13 ]. We wondered whether dural acid treatment induced trigeminal pain in mice through ASICs or TRPV1. To address this question, we assessed acid-induced nocifensive behaviour in mice treated with either amiloride (an ASICs antagonist) or AMG-9810 (a TRPV1 antagonist). We quantified the duration of both forepaw wiping and hind paw scratching as well as the expression of c-FOS expression in the Sp5C. Co-treatment of AMG-9810 did not alter the dural acid-induced trigeminal pain behaviour. In contrast, co-treatment with amiloride blocked the nocifensive behaviour elicited by dural administration of pH 6.0 SIF alone.

Only forepaw wiping converse black high tops was significantly less robust in mice co-treated with KN-93 than mice treated with pH 6.0 SIF alone and KN-93 had no effect on hind paw scratching (Fig.  5 B).Moreover, co-treatment with KN-93 also attenuated c-FOS expression, the expression of c-FOS in the Sp5C in the KN-93 group was significantly lower than that in the pH 6.0 SIF alone group (Fig.  5 C, D).Dural co-administration of the ASICs antagonist amiloride effectively inhibited the acid-induced behaviour, but the specific TRPV1 antagonist AMG-9810 failed to impact the behaviour, suggesting that ASICs may be related to the on-going trigeminal pain in this model.

Furthermore, cortical spreading depression has been shown to be accompanied by dural ischaemia, which can produce a drop in dural pH to activate ASICs and initiate signalling in migraine [ 19 , 22 ].Moreover, activation of the CaMKII/CREB signalling pathway is necessary for the acid-induced mouse behaviour, as evidenced by the inhibitory effect of systemically administered KN-93. It is possible that increased Ca2 influx via activation of ASICs may regulate many intracellular Ca2 -dependent signalling pathways by altering the physiological function of multiple Ca2 binding proteins, amongst which CaMKII is a converse trainers likely candidate [ 23 , 24 ].

The nociceptive transcription factor CREB is essential for the regulation of pro-nociceptive genes, such as c-FOS. In our study, the inhibition of CaMKII significantly blocked the increase in the gene expression of c-FOS induced by the acidic solution.Chronic intermittent treatment with acidic solution alone produces chronic hypersensitivity that represents a model of trigeminal pain. ASIC1a and ASIC3 levels are significantly elevated in acid-induced trigeminal nociceptive pathways, which contribute to the development of recurrent trigeminal pain through the activation of the CaMKII/CREB signalling pathway. Inhibitors [تصویر:  converse%20trainers-172wcu.jpg] of ASICs may serve as novel candidates for migraine therapy.
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