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signaling of sAPP may perhaps involve other factors which a

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signaling of sAPP may perhaps involve other factors which a

Сообщение  qq123456 в Ср Апр 27, 2016 10:20 am

In contrast, INNO-406 溶解度 intrathecal administration of cars didn't modify the withdrawal threshold. Discussion This research demonstrates that intrathecal administration of MRS2578 and NF340 partially reverses spinal nerve damage induced tactile allodynia. Considering the fact that these drugs are selective P2Y6 and P2Y11 receptor antagonists, respectively, our data suggest that the two spinal receptors participate in the upkeep of neuropathic discomfort induced by spinal nerve injury. Our success agree that has a former re port exhibiting that intrathecal administration of MRS2578 suppresses spared nerve injury induced mechanical allody nia, suggesting that spinal P2Y6 receptors participate in the upkeep of neuropathic discomfort.<br><br> Nevertheless, our information disagree with other review demonstrating that P2Y6 re ceptors play an antinociceptive purpose as intrathecal uridine diphosphate administration displays antiallodynic results following partial sciatic nerve ligation. This discrepancy may very well be explained on the basis of Lapatinib 分子量 the employed P2Y6 receptor agonist selectivity as UDP also activates the P2Y14 receptor with higher affinity than for P2Y6 receptors. In our examine we demonstrated that intrathecal administration of your selective P2Y6 and P2Y11 receptor agonists creates lengthy lasting tactile allodynia which argues against the antinocicep tive impact of spinal P2Y6 receptors. Regarding NF340, this appears to be the very first report demonstrating the antinociceptive result of this compound suggesting that spinal P2Y11 receptors play an important purpose from the servicing of neuropathic soreness.<br><br> The contribu tion of P2Y6 receptors LY2109761 700874-71-1 seems to be unique from that of P2Y11 receptors since the P2Y6 receptor antagonist developed a peak in the antiallodynic impact in about 12 h after which decayed rapidly. In contrast, the P2Y11 receptor antagonist generated a modest but sustained antiallodynic impact. This discrepancy may be due to distinctions in the pharmacokinetics or pharmacodynamics from the examined drugs. Taken with each other, our information suggest the participation of spinal P2Y6,eleven receptors from the mainten ance of neuropathic ache. In support to our pharmacological examine, we demon strated by western blot that P2Y6,eleven receptors are expressed during the dorsal spinal cord of na ve rats.<br><br> Earlier studies indicate that P2Y6 receptor mRNA is discovered in rat micro glia. To the contrary, P2Y11 receptors have only been described in people. Presently there are no reports of a cloned P2Y11 receptor in rats. Even so, this receptor has become recently reported in epithelial cells, principal glial cells, lacrimal glands, neutrophils, and brain of rats. So, our data recommend the P2Y6 receptor is expressed and fully practical inside the spinal cord. On top of that, our success suggest the presence of a P2Y11like receptor inside the rat spinal cord. Moreover their presence in na ve animals, P2Y6,eleven receptors expression from the ipsilateral dorsal spinal cord was up regulated at 7 and 14 days just after spinal nerve ligation. These benefits partially agree having a preceding study showing that P2Y6 receptor mRNA is up regulated in the ipsilateral spinal cord at three days following peripheral nerve damage.


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