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anti rat p2x3 receptor  (Alomone Labs)


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    Structured Review

    Alomone Labs anti rat p2x3 receptor
    Daily i.t. injection of the selective <t>P2X3</t> receptor antagonist A317491 attenuates morphine‐induced anti‐nociceptive tolerance. (A) Schematic of the experimental timeline. (B) Thermal and (C) mechanical thresholds measured daily in all groups (n = 6; *P < 0.05 vs. saline group; # P < 0.05 vs. morphine group).
    Anti Rat P2x3 Receptor, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti rat p2x3 receptor/product/Alomone Labs
    Average 92 stars, based on 6 article reviews
    anti rat p2x3 receptor - by Bioz Stars, 2026-02
    92/100 stars

    Images

    1) Product Images from "Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia"

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    Journal: British Journal of Pharmacology

    doi: 10.1111/bph.14191

    Daily i.t. injection of the selective P2X3 receptor antagonist A317491 attenuates morphine‐induced anti‐nociceptive tolerance. (A) Schematic of the experimental timeline. (B) Thermal and (C) mechanical thresholds measured daily in all groups (n = 6; *P < 0.05 vs. saline group; # P < 0.05 vs. morphine group).
    Figure Legend Snippet: Daily i.t. injection of the selective P2X3 receptor antagonist A317491 attenuates morphine‐induced anti‐nociceptive tolerance. (A) Schematic of the experimental timeline. (B) Thermal and (C) mechanical thresholds measured daily in all groups (n = 6; *P < 0.05 vs. saline group; # P < 0.05 vs. morphine group).

    Techniques Used: Injection

    (A) Expression of P2X3 receptor and (B) number of P2X3 receptor‐positive cells per section per animal in DRGs increase after repeated morphine treatment. The DRGs were removed 2 h after morphine injection on day 7 (n = 6,*P < 0.05 vs. saline (S) group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.
    Figure Legend Snippet: (A) Expression of P2X3 receptor and (B) number of P2X3 receptor‐positive cells per section per animal in DRGs increase after repeated morphine treatment. The DRGs were removed 2 h after morphine injection on day 7 (n = 6,*P < 0.05 vs. saline (S) group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Techniques Used: Expressing, Injection

    Morphine‐induced P2X3 receptor up‐regulation is co‐localized with IB4 and peripherin in the DRG. (A) Confocal images of P2X3 receptor (green) and ionized Ca2+‐binding adapter molecule 1 (Iba1) (red) immunofluorescence with no co‐localization. (B) Immunofluorescence images of P2X3 receptor (red) and IB4 (green) co‐localization in DRGs. (C) There was less co‐localization of P2X3 receptor (green) with NF200 (red) in myelinated neurons. (D) Co‐localization of P2X3 receptor (green) with peripherin (red) in unmyelinated/small‐calibre neurons. DRG samples from the 7 day morphine group (scale bars: A/B, 80 μm; C/D, 20 μm).
    Figure Legend Snippet: Morphine‐induced P2X3 receptor up‐regulation is co‐localized with IB4 and peripherin in the DRG. (A) Confocal images of P2X3 receptor (green) and ionized Ca2+‐binding adapter molecule 1 (Iba1) (red) immunofluorescence with no co‐localization. (B) Immunofluorescence images of P2X3 receptor (red) and IB4 (green) co‐localization in DRGs. (C) There was less co‐localization of P2X3 receptor (green) with NF200 (red) in myelinated neurons. (D) Co‐localization of P2X3 receptor (green) with peripherin (red) in unmyelinated/small‐calibre neurons. DRG samples from the 7 day morphine group (scale bars: A/B, 80 μm; C/D, 20 μm).

    Techniques Used: Binding Assay, Immunofluorescence

    Involvement of PKCε in morphine (Mor)‐induced antinociceptive tolerance and P2X3 receptor expression. (A) The phosphorylation of PKCε in the DRG increased time dependently with chronic Mor treatment. (B) The inhibitor of PKCε, ε‐V1‐2, reversed the increased P2X3 receptor expression induced by repeated Mor treatment. (C) PKCε co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the up; 20 μm for the down). (D) Mor tolerance was attenuated when Mor was administered with ε‐V1‐2 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.
    Figure Legend Snippet: Involvement of PKCε in morphine (Mor)‐induced antinociceptive tolerance and P2X3 receptor expression. (A) The phosphorylation of PKCε in the DRG increased time dependently with chronic Mor treatment. (B) The inhibitor of PKCε, ε‐V1‐2, reversed the increased P2X3 receptor expression induced by repeated Mor treatment. (C) PKCε co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the up; 20 μm for the down). (D) Mor tolerance was attenuated when Mor was administered with ε‐V1‐2 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Techniques Used: Expressing, Injection

    Epac is responsible for the chronic morphine (Mor)‐induced phosphorylation of PKCε and increase in P2X3 receptor expression. (A) The expression of Epac in the DRG increased time dependently after chronic Mor exposure. (B) The inhibitor of Epac, ESI‐09, reversed the increased P2X3 receptor expression and phosphorylation of PKCε induced by repeated morphine treatment. (C) Epac co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the left; 20 μm for the right). (D) Morphine tolerance was attenuated by co‐administration of morphine and ESI‐09 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.
    Figure Legend Snippet: Epac is responsible for the chronic morphine (Mor)‐induced phosphorylation of PKCε and increase in P2X3 receptor expression. (A) The expression of Epac in the DRG increased time dependently after chronic Mor exposure. (B) The inhibitor of Epac, ESI‐09, reversed the increased P2X3 receptor expression and phosphorylation of PKCε induced by repeated morphine treatment. (C) Epac co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the left; 20 μm for the right). (D) Morphine tolerance was attenuated by co‐administration of morphine and ESI‐09 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Techniques Used: Expressing, Injection



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    Image Search Results


    Daily i.t. injection of the selective P2X3 receptor antagonist A317491 attenuates morphine‐induced anti‐nociceptive tolerance. (A) Schematic of the experimental timeline. (B) Thermal and (C) mechanical thresholds measured daily in all groups (n = 6; *P < 0.05 vs. saline group; # P < 0.05 vs. morphine group).

    Journal: British Journal of Pharmacology

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    doi: 10.1111/bph.14191

    Figure Lengend Snippet: Daily i.t. injection of the selective P2X3 receptor antagonist A317491 attenuates morphine‐induced anti‐nociceptive tolerance. (A) Schematic of the experimental timeline. (B) Thermal and (C) mechanical thresholds measured daily in all groups (n = 6; *P < 0.05 vs. saline group; # P < 0.05 vs. morphine group).

    Article Snippet: Membranes were incubated with the following primary antibodies: rabbit anti‐rat P2X3 receptor (1:1000; Alomone Labs, Jerusalem, Israel), mouse anti‐GAPDH (1:1000; CST, Danvers, MA, USA), rabbit anti‐rat pPKCε (1:1000; Abcam, Cambridge, MA, USA), mouse anti‐rat PKCε (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and mouse anti‐rat Epac (1:200; Santa Cruz Biotechnology).

    Techniques: Injection

    (A) Expression of P2X3 receptor and (B) number of P2X3 receptor‐positive cells per section per animal in DRGs increase after repeated morphine treatment. The DRGs were removed 2 h after morphine injection on day 7 (n = 6,*P < 0.05 vs. saline (S) group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Journal: British Journal of Pharmacology

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    doi: 10.1111/bph.14191

    Figure Lengend Snippet: (A) Expression of P2X3 receptor and (B) number of P2X3 receptor‐positive cells per section per animal in DRGs increase after repeated morphine treatment. The DRGs were removed 2 h after morphine injection on day 7 (n = 6,*P < 0.05 vs. saline (S) group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Article Snippet: Membranes were incubated with the following primary antibodies: rabbit anti‐rat P2X3 receptor (1:1000; Alomone Labs, Jerusalem, Israel), mouse anti‐GAPDH (1:1000; CST, Danvers, MA, USA), rabbit anti‐rat pPKCε (1:1000; Abcam, Cambridge, MA, USA), mouse anti‐rat PKCε (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and mouse anti‐rat Epac (1:200; Santa Cruz Biotechnology).

    Techniques: Expressing, Injection

    Morphine‐induced P2X3 receptor up‐regulation is co‐localized with IB4 and peripherin in the DRG. (A) Confocal images of P2X3 receptor (green) and ionized Ca2+‐binding adapter molecule 1 (Iba1) (red) immunofluorescence with no co‐localization. (B) Immunofluorescence images of P2X3 receptor (red) and IB4 (green) co‐localization in DRGs. (C) There was less co‐localization of P2X3 receptor (green) with NF200 (red) in myelinated neurons. (D) Co‐localization of P2X3 receptor (green) with peripherin (red) in unmyelinated/small‐calibre neurons. DRG samples from the 7 day morphine group (scale bars: A/B, 80 μm; C/D, 20 μm).

    Journal: British Journal of Pharmacology

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    doi: 10.1111/bph.14191

    Figure Lengend Snippet: Morphine‐induced P2X3 receptor up‐regulation is co‐localized with IB4 and peripherin in the DRG. (A) Confocal images of P2X3 receptor (green) and ionized Ca2+‐binding adapter molecule 1 (Iba1) (red) immunofluorescence with no co‐localization. (B) Immunofluorescence images of P2X3 receptor (red) and IB4 (green) co‐localization in DRGs. (C) There was less co‐localization of P2X3 receptor (green) with NF200 (red) in myelinated neurons. (D) Co‐localization of P2X3 receptor (green) with peripherin (red) in unmyelinated/small‐calibre neurons. DRG samples from the 7 day morphine group (scale bars: A/B, 80 μm; C/D, 20 μm).

    Article Snippet: Membranes were incubated with the following primary antibodies: rabbit anti‐rat P2X3 receptor (1:1000; Alomone Labs, Jerusalem, Israel), mouse anti‐GAPDH (1:1000; CST, Danvers, MA, USA), rabbit anti‐rat pPKCε (1:1000; Abcam, Cambridge, MA, USA), mouse anti‐rat PKCε (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and mouse anti‐rat Epac (1:200; Santa Cruz Biotechnology).

    Techniques: Binding Assay, Immunofluorescence

    Involvement of PKCε in morphine (Mor)‐induced antinociceptive tolerance and P2X3 receptor expression. (A) The phosphorylation of PKCε in the DRG increased time dependently with chronic Mor treatment. (B) The inhibitor of PKCε, ε‐V1‐2, reversed the increased P2X3 receptor expression induced by repeated Mor treatment. (C) PKCε co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the up; 20 μm for the down). (D) Mor tolerance was attenuated when Mor was administered with ε‐V1‐2 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Journal: British Journal of Pharmacology

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    doi: 10.1111/bph.14191

    Figure Lengend Snippet: Involvement of PKCε in morphine (Mor)‐induced antinociceptive tolerance and P2X3 receptor expression. (A) The phosphorylation of PKCε in the DRG increased time dependently with chronic Mor treatment. (B) The inhibitor of PKCε, ε‐V1‐2, reversed the increased P2X3 receptor expression induced by repeated Mor treatment. (C) PKCε co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the up; 20 μm for the down). (D) Mor tolerance was attenuated when Mor was administered with ε‐V1‐2 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Article Snippet: Membranes were incubated with the following primary antibodies: rabbit anti‐rat P2X3 receptor (1:1000; Alomone Labs, Jerusalem, Israel), mouse anti‐GAPDH (1:1000; CST, Danvers, MA, USA), rabbit anti‐rat pPKCε (1:1000; Abcam, Cambridge, MA, USA), mouse anti‐rat PKCε (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and mouse anti‐rat Epac (1:200; Santa Cruz Biotechnology).

    Techniques: Expressing, Injection

    Epac is responsible for the chronic morphine (Mor)‐induced phosphorylation of PKCε and increase in P2X3 receptor expression. (A) The expression of Epac in the DRG increased time dependently after chronic Mor exposure. (B) The inhibitor of Epac, ESI‐09, reversed the increased P2X3 receptor expression and phosphorylation of PKCε induced by repeated morphine treatment. (C) Epac co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the left; 20 μm for the right). (D) Morphine tolerance was attenuated by co‐administration of morphine and ESI‐09 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Journal: British Journal of Pharmacology

    Article Title: Exchange factor directly activated by cAMP–PKCε signalling mediates chronic morphine‐induced expression of purine P2X3 receptor in rat dorsal root ganglia

    doi: 10.1111/bph.14191

    Figure Lengend Snippet: Epac is responsible for the chronic morphine (Mor)‐induced phosphorylation of PKCε and increase in P2X3 receptor expression. (A) The expression of Epac in the DRG increased time dependently after chronic Mor exposure. (B) The inhibitor of Epac, ESI‐09, reversed the increased P2X3 receptor expression and phosphorylation of PKCε induced by repeated morphine treatment. (C) Epac co‐localized with P2X3 receptor in DRGs (scale bar: 50 μm for the left; 20 μm for the right). (D) Morphine tolerance was attenuated by co‐administration of morphine and ESI‐09 for 7 days (n = 6,*P < 0.05 vs. saline (S) group; # P < 0.05 vs. morphine group). M3, 3 days of morphine injection; M5, 5 days of morphine injection; M7, 7 days of morphine injection.

    Article Snippet: Membranes were incubated with the following primary antibodies: rabbit anti‐rat P2X3 receptor (1:1000; Alomone Labs, Jerusalem, Israel), mouse anti‐GAPDH (1:1000; CST, Danvers, MA, USA), rabbit anti‐rat pPKCε (1:1000; Abcam, Cambridge, MA, USA), mouse anti‐rat PKCε (1:200; Santa Cruz Biotechnology, Santa Cruz, CA, USA) and mouse anti‐rat Epac (1:200; Santa Cruz Biotechnology).

    Techniques: Expressing, Injection