Showing posts with label P2X3 Receptor Antibody. Show all posts
Showing posts with label P2X3 Receptor Antibody. Show all posts

Thursday, May 27, 2021

Trigeminal Neuralgia (Facial Pain)

 Markers for Pain Research

Trigeminal Neuralgia is a progress chronic condition. Dysfunctional trigeminal signaling can lead to intense, searing facial pain. It is caused by pressure on the trigeminal nerve.

The root causes of the condition are not well understood. Our pain research markers have been widely used and frequently published through the years and have been important contributors to our growth, Here's a recent pub referencing use of one our P2X3 Antibodies-Momoko Koizumi, Sayaka Asano, Akihiko Furukawa, Yoshinori Hayashi, Suzuro Hitomi, Ikuko Shibuta, Katsuhiko Hayashi, Fusao Kato, Koichi Iwata, and Masamichi Shinoda. (2021). P2X3 Receptor Upregulation in Trigeminal Ganglion Neurons Through TNFα Production in Macrophages Contributes to Trigeminal Neuropathic Pain in Rats. The Journal of Headache and Pain, 22, 31. doi: 10.1186/s10194-021-01244-4

Images: Changes in P2X3R expression in TG neurons innervating whisker pad skin and the involvement of P2X3R signaling in TG neurons in orofacial mechanical hypersensitivity on day 7 following TNC. a Photomicrograph of FG-labeled P2X3IR TG neurons following the TNC or sham procedure. Arrows indicate FG-labeled P2X3IR TG neurons. Scale bar: 100 μm. b Mean number of FG-labeled TG neurons ipsilateral to the TNC or sham procedure (n = 5 in each). c The frequency of FG-labeled P2X3-IR TG neurons ipsilateral to the TNC or sham procedure. * p < 0.05 vs. sham. (n = 5 in each, student’s t-test). d The time course of changes in the MHWT by subcutaneous A317491 or TNP-ATP administration on day 7 following the TNC or sham procedure.


The signaling of TNFα released from the activated macrophages and infiltrated into and/or proliferated in the TG induces the upregulation of P2X3R expression in TG neurons innervating the orofacial region, resulting in orofacial mechanical allodynia following TNC. Consequently, TG neuronal P2X3R hyperexpression by enhanced TNFα signaling in the TG is a potential target for TN treatment..

Monday, November 17, 2014

Neuropathy Research Solutions

New Publications and Past Postings

Here're are several key postings on Neuropathy and Neuropathic Pain:
Here're some "hot of the press" publications referencing use of Neuron-Glial Markers: 
Bethany L. Johnson-Kerner, Faizzan S. Ahmad, Alejandro Garcia Diaz, J. Palmer Greene, Steven J. Gray, R. Jude Samulski, Wendy K. Chung, Rudy Van Coster, Paul Maertens, Scott A. Noggle, Christopher E. Henderson and Hynek Wichterle. Intermediate filament protein accumulation in motor neurons derived from giant axonal neuropathy iPSCs rescued by restoration of gigaxonin. Hum. Mol. Genet. (2014) doi: 10.1093/hmg/ddu556. First published online: November 4, 2014.
...MAP2 (1:2,000, Neuromics, CH22103), NF-H (1:2000, Neuromics, CH22104), NF-L (1:200, Neuromics, MO22104)...

Images: Cells grown from adult rat brain. Large cell in middle is stained with mouse monoclonal to NF-L clone DA2 (green). Another type of neuronal lineage cell was stained with rabbit polyclonal to alpha-internexin (red). These cells were mitotic but had several characteristics of neurons. Rat spinal cord homogenate showing the major intermediate filament proteins of the nervous system (lane 1). The remaining lanes show blots of this material stainted with various antibodies including: NF-H, NF-M,, NF-L,, NF66 and GFAP 

Jianfei Guo, Xudong Fu, Xia Cui, Minhua Fan. Contributions of purinergic P2X3 receptors within the midbrain periaqueductal gray to diabetes-induced neuropathic pain. The Journal of Physiological Sciences November 2014.
...An equal volume of total and membrane samples was applied to SDS-PAGE. Membranes were incubated with the rabbit anti-P2X 3 primary antibody (1:1000, Neuromics, Edina, MN, USA) and goat anti-rabbit secondary antibody (1:200, Neuromics, Edina, MN, USA).

Neuropathy Research Solutions Include:


Saturday, October 12, 2013

P2X3 Receptor and Inflammatory Nociception

P2X3 Activates TRPA1, 5-HT3 and 5-HT1A Receptors

Endogenous ATP via activation of P2X3 Receptors contributes to inflammatory nociception in different models, including the formalin injected in subcutaneous tissue of the rat's hind paw. In this study, researchers evaluated whether TRPA1, 5-HT3 and 5-HT1A receptors, whose activation is essential to formalin-induced inflammatory nociception, are involved in the nociception induced by activation of P2X3 receptors on subcutaneous tissue of the rat's hind paw: Suzy Krimon, Dionéia Araldi, Filipe César do Prado, Cláudia Herrera Tambeli, Maria Cláudia G. Oliveira-Fusaro, Carlos Amílcar Parada. P2X3 receptors induced inflammatory nociception modulated by TRPA1, 5-HT3 and 5-HT1A receptors. Pharmacology Biochemistry and Behavior, Available online 8 October 2013. http://dx.doi.org/10.1016/j.pbb.2013.09.017. Our widely used and frequently published P2X3 R Antibody places a central role in measuring the expression of the protein...containing 5% non-fat dry milk at room temperature, followed by incubation with P2X3 rabbit polyclonal antibody (1:500; Neuromics) overnight at 4 °C, rinsed six times with TBST, and then incubated for 40 minutes in goat anti-rabbit IgG peroxidase...
Image: Neuromics' P2X3 R WB Example: Sequence‐specific siRNA‐mediated repression of P2X3. (A) P2X3 mRNA inhibition by 200 nM siRNA duplexes. Twenty‐four hours after transfection of CHO‐rP2X3 cells, P2X3‐specific mRNA was measured with Q‐PCR and plotted as percentage of mRNA detected in the control treated with Oligofectamine alone. Sequences and modifications are shown in Figure 1B and Table 1. (B) P2X3 protein reduction by 200 nM siRNA‐8646/8647, but not by its mismatch analogue siRNA‐MM‐7558/7559 or the unrelated siRNA‐7126/7127. Twenty‐four hours after transfection, protein was extracted and analysed by western blotting. P2X3‐specific immunodetection reveals expression levels as shown below (an average value from two experiments). Time points as indicated at the top. Molecular weights of two glycosylated forms of P2X3 are shown on the left. 

Conclusions: Nociceptive response intensity was measured by observing the rat's behavior and considering the number of times the animal reflexively raised its hind paw (flinches) in 60 min. Local subcutaneous administration of the selective TRPA1, 5-HT3 or 5-HT1A receptor antagonists HC 030031, tropisetron and WAY 100,135, respectively, prevented the nociceptive responses induced by the administration in the same site of the non-selective P2X3 receptor agonist αβmeATP. Administration of the selective P2X3 and P2X2/3 receptor antagonist A-317491 or pretreatment with oligonucleotides antisense against P2X3 receptor prevented the formalin-induced behavioral nociceptive responses during the first and second phases. Also, the co-administration of a subthreshold dose of αβmeATP with a subthreshold dose of formalin induced nociceptive behavior, which was prevented by local administration of tropisetron, HC 030031 or WAY 100, 135. These findings have demonstrated that the activation of P2X3 receptors induces inflammatory nociception modulated by TRPA1, 5-HT3 and 5-HT1A receptors. Also, they suggest that inflammatory nociception is modulated by the release of endogenous ATP and P2X3 receptor activation, which in turn, increases primary afferent nociceptor susceptibility to the action of inflammatory mediators via interaction with TRPA1, 5-HT3 and 5-HT1A receptors in the peripheral tissue.

I will continue to post pain and inflammation related studies that reference the use of our antibodies.