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MessagePosté le: Mar 1 Juil - 07:07 (2014) Sujet du message: Unlike DEG approach, GSEA uses the whole gene expression da Répondre en citant

 On the other hand, TRPV1 receptors do not appear to play a crucial role in the onset of TH in this model. In addition, we also concluded that ASICs did not contribute to thermal hypersensitivity in AS TIIP rats. AP24534 臨床試験 Previously, we reported that peripheral ASICs were involved in maintaining ischemia induced mechan ical allodynia in TIIP. However, we were unable to in vestigate their contribution to TH in the present study, since TIIP rats have normal heat sensitivity. In the current study, we observed that low tissue pH in conjunction with ischemia resulted in the development of TH in TIIP rats, and ASICs were not involved in this ischemic thermal hypersensitivity. On the other hand, ASICs did contribute to mechanical allodynia in AS TIIP rats.

These results suggest that ASICs are supplier AT7519 a modality specific contributor to mechanical allodynia in acid induced nociception, and there are several reports supporting the specific role of ASICs in mechanical sensing and hypersensitivity. Although pH 4. 0 is quite an extreme pH not often seen even in pathophysiological conditions, several stud ies have examined the actual pH level in the plantar tis sue, and they demonstrated that the measured tissue pH is considerably higher than solution pH level before in jection. For example, Sluka et al. reported that the repeated injection of pH 4. 0 saline into gastrocne mius muscle lowered the muscle pH averaged 6. 5 with decreases in individual animals to pH 6. Therefore, we have assumed that a single injection of pH 4. 0 saline would not extremely decrease the tissue pH, and further considered that temporary acidic pH tissue condition in duced by pH 4.

0 saline could mimic the pathophysio logical state shown in peripheral ischemic condition. Collectively, the acidic environment is easily buffered by physiological buffering systems, it may be dif ficult to activate TRPV1 receptors directly, since they only respond under relatively reversible Akt 阻害剤 low tissue pH. Therefore, there is the strong possibility that the interaction of the acidic environment and ATP indirectly activate TRPV1 via P2Y1 receptors which up regulates intracellular signaling cascades, but this only occurs in an ischemic environment in which tissue acidosis is present. It is well recognized that activation of TRPV1 recep tors contributes to peripheral sensitization, particularly to heat stimuli.

Pro algesic substances such as protons, ATP, bradykinin and prostaglandins sensitize nociceptors either by directly modulating the sensitivity of mem brane receptors or by up regulating intracellular signal ing cascades. These signaling cascades include calcium dependent protein kinase, cyclic AMP dependent protein kinase, and calcium calmodulin dependent protein kinase dependent phosphorylation. Since PKC dependent modulation of TRPV1 had been re ported to be the main pathway stimulated by inflamma tory mediators, an analysis of phosphorylated TRPV1 that targeted S800 was performed in the present study. Sham, TIIP and AS TIIP rats did not show any alterations in TRPV1 expression, whereas the ratio of pTRPV1 TRPV1 was significantly ele vated in AS TIIP rats.


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MessagePosté le: Mar 1 Juil - 07:07 (2014) Sujet du message: Publicité

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