Showing posts with label Hyperalgesia. Show all posts
Showing posts with label Hyperalgesia. Show all posts

Tuesday, June 24, 2014

More Gains on Pain Research

Discovering the Related Pathways

There are multiple descriptions for chronic and acute pain: stabbing, burning, cutting, itching, numbing, crushing and more. Understanding the pathways are important to optimizing the therapies and treatments for the many different forms of pain.

The foundation of Neuromics is providing top notch pain research markers, gene expression analysis tools and cell based assays. Here I share recent publications from customers using these:
Inflammatory Joint Pain: Fiona B Carr, Sandrine M Géranton and Stephen P Hunt. Descending controls modulate inflammatory joint pain and regulate CXC chemokine and iNOS expression in the dorsal horn. Molecular Pain 2014, 10:39 doi:10.1186/1744-8069-10-39...mu opioid receptor, 1:10,000, Neuromics (RA10104)...

Images: Representative single plane confocal images of MOR immunohistochemistry in the 1.5pmole dermorphin-saporin group and saline control. Double labelling with NeuN indicated that although many MOR+ neurons are depleted at this dose, some surviving MOR- neurons remain in the region, indicated by white arrows. Scale bars indicate 25 µm

Temperature Sensation: Marics I, Malapert P, Reynders A, Gaillard S, Moqrich A (2014) Acute Heat-Evoked Temperature Sensation Is Impaired but Not Abolished in Mice Lacking TRPV1 and TRPV3 Channels. PLoS ONE 9(6): e99828. doi:10.1371/journal.pone.0099828. ...TRPV1 antibody (1/1000 dilution, Neuromics)...

Acute PainPaulino Barragán-Iglesias, Hector I. Rocha-González, Jorge Baruch Pineda-Farias, Janet Murbartián, Beatriz Godínez-Chaparro, Peter S. Reinach, Thiago M. Cunha, Fernando Q. Cunha, Vinicio Granados-Soto, Inhibition of peripheral anion exchanger 3 decreases formalin-induced pain, European Journal of Pharmacology, Available online 27 May 2014, ISSN 0014-2999, http://dx.doi.org/10.1016/j.ejphar.2014.05.029. (http://www.sciencedirect.com/science/article/pii/S0014299914003914). ...substance P (guinea pig; 1:200; Cat # GP14110; Neuromics, Edina, MN), and purinergic P2×3 receptor (guinea pig: 1:1000; Cat # GP10108 ...

We are pleased with the many publications and customer provided data proving the quality of our many pain research tools. I am always available to serve you, Pete Shuster (pshuster@neuromics.com) or direct phone: 612-801-1007.

Sunday, May 20, 2012

Cannabinoid Type-1 Receptors and Chemotherapy Related Pain

Chemotherapy can induce painful peripheral neuropathy and also have a toxic effect on peripheral nerves. The authors here show that that cisplatin produces hyperalgesia and toxicity to sensory neurons as indicated by neurochemical, morphological, and functional measures. Increasing AEA signaling at CB1 receptors not only reduced the hyperalgesia but reduced the neurotoxicity of cisplatin as well:  Iryna A. Khasabova,Sergey Khasabov, Justin Paz, Catherine Harding-Rose, Donald A. Simone, and Virginia S. Seybold. Cannabinoid Type-1 Receptor Reduces Pain and Neurotoxicity Produced by Chemotherapy. The Journal of Neuroscience, 16 May 2012, 32(20): 7091-7101; doi: 10.1523/​JNEUROSCI.0403-12.2012.

The authors use our guinea pig TRPV1 antibody to measure cisplatin hyperalgesia vs treated and control mice.

Images: URB597 attenuated effects of cisplatin on protein expression in DRGs. A, TRPV1- and ATF-3-ir were detected by immunofluorescence in L3–L5 DRGs from mice treated with vehicle, cisplatin, or cisplatin plus URB597. Cisplatin (1 mg/kg of body weight, daily for 7 d, i.p.) increased the occurrence of TRPV1- and ATF3-ir in neurons. Co-injection of URB597 (0.3 mg/kg daily, i.p.) with cisplatin attenuated the effect cisplatin on protein-ir. Scale bars: 10 μm (for images within each antigen). B, Quantitative summary of the effect of treatments on TRPV1-ir in neurons. Data are expressed as the mean ± SEM. aSignificantly different from each other group (p < 0.05, one-way ANOVA with Student–Newman–Keuls test; n = 4 mice/treatment). C, Quantitative summary of the effect of treatments on ATF-ir in neurons. Data are expressed as the median and 25th and 75th percentile range. *Significantly different from vehicle control and cisplatin plus URB597 groups (n = 6 mice/treatment; p < 0.001, Kruskal–Wallis ANOVA on ranks test).

Related Reagents:

VR1 N-Terminus (TRPV1)
VR1 (TRPV1)-Goat
VR1 C-Terminus (TRPV1) - mouse specific
All TRP Antibodies
Pain and Inflammation Research Antibodies
Neurotransmission -Neurotransmission Research Antibody Categories

Saturday, January 15, 2011

Upregulations of P2X3 and ASIC3 involve in hyperalgesia

It gets my attention when several of our ion channel markers are referenced in the title of a publication.

Kiyomi Hori, Noriyuki Ozaki, Shigeyuki Suzuki, Yasuo Sugiura. Upregulations of P2X3 and ASIC3 involve in hyperalgesia induced by cisplatin administration in rats. PAIN 149 (2010) 393–405

Findings: "We explored the role of ion channels expressed in DRG neurons in the painful neuropathy associated with cisplatin administration. Upregulations of TRPV2, P2X3 and ASIC3 may play important roles in the mechanical hyperalgesia induced by cisplatin. In addition to cutaneous hyperalgesia, cisplatin treatment might also induce muscle hyperalgesia associated with upregulations of P2X3 and
ASIC3. Interfering with these channels may prove to be a promising therapeutic target for treating painful symptoms of cisplatin neuropathy, and may further be able to ensure the continuation of anticancer therapy."

Images: ASIC3 (Dilution 1:10) amd P2X3 (Dilution 1:500) satining of rat Dorsal Root Ganglia (DRGs) of cisplatin-treated animals. After dilution in 0.1 M phosphate-buffered saline (PBS) containing 1.5% normal goat serum and 0.3% Triton X-100 (Sigma), DRG sections were incubated with either guinea pig polyclonal antiserum against synthetic rat ASIC3 and rabbit polyclonal antiserum against synthetic rat P2X3 (1:500; Neuromics). The sections for ASIC3 were reacted with reagents for 2 days at room temperature and others at 4OC. After being rinsed with 0.1 M PBS, the sections were reacted in PBS with fluorescein-isothiocyanate (FITC)-conjugated goat anti-guinea pig or - rabbit IgG antibody (Vector Laboratories, Burlingame, CA, USA) at a concentration of 1:100. After being rinsed with 0.1 M PBS, the sections were cover-slipped in mounting medium (Immunon, Pittsburgh, PA, USA) and examined under a fluorescence microscope equipped with a digital camera