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p2x7 primary antibody  (Alomone Labs)


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    Alomone Labs p2x7 primary antibody
    The role of <t>P2X7</t> receptors in the hypertensive kidney. P2X7 receptors are non-selective cation channel receptors activated by extracellular adenosine triphosphate (ATP). P2X7 receptors are abundantly expressed by immune cells, such as macrophages. ATP released by damaged or activated cells activates P2X7 receptors on macrophages to mediate NOD−, LRR− and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and caspase-1 assembly leading to inflammasome activation, and the subsequent maturation and release of pro-inflammatory cytokines such as interleukin (IL)-1β. These cytokines promote renal interstitial inflammation and promote sodium retention by tubular epithelial cells, thereby contributing to salt-sensitivity and hypertension. P2X7 receptors are also expressed in renal vascular endothelial cells, particularly in the pre-glomerular vasculature and vasa recta . ATP, released by endothelial cells, can activate endothelial P2X7 receptors in an autocrine/paracrine fashion to promote vasoconstriction, ultimately decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). Figure contains a modified illustration from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License ( https://creativecommons.org/licenses/by/4.0/ ).
    P2x7 Primary Antibody, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 96/100, based on 214 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p2x7+primary+antibody/Anti-P2X7+Receptor+Antibody/pmc11053004-78-18-23
    Average 96 stars, based on 214 article reviews
    p2x7 primary antibody - by Bioz Stars, 2026-09
    96/100 stars

    Images

    1) Product Images from "P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats"

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    Journal: Scientific Reports

    doi: 10.1038/s41598-024-59635-x

    The role of P2X7 receptors in the hypertensive kidney. P2X7 receptors are non-selective cation channel receptors activated by extracellular adenosine triphosphate (ATP). P2X7 receptors are abundantly expressed by immune cells, such as macrophages. ATP released by damaged or activated cells activates P2X7 receptors on macrophages to mediate NOD−, LRR− and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and caspase-1 assembly leading to inflammasome activation, and the subsequent maturation and release of pro-inflammatory cytokines such as interleukin (IL)-1β. These cytokines promote renal interstitial inflammation and promote sodium retention by tubular epithelial cells, thereby contributing to salt-sensitivity and hypertension. P2X7 receptors are also expressed in renal vascular endothelial cells, particularly in the pre-glomerular vasculature and vasa recta . ATP, released by endothelial cells, can activate endothelial P2X7 receptors in an autocrine/paracrine fashion to promote vasoconstriction, ultimately decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). Figure contains a modified illustration from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License ( https://creativecommons.org/licenses/by/4.0/ ).
    Figure Legend Snippet: The role of P2X7 receptors in the hypertensive kidney. P2X7 receptors are non-selective cation channel receptors activated by extracellular adenosine triphosphate (ATP). P2X7 receptors are abundantly expressed by immune cells, such as macrophages. ATP released by damaged or activated cells activates P2X7 receptors on macrophages to mediate NOD−, LRR− and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and caspase-1 assembly leading to inflammasome activation, and the subsequent maturation and release of pro-inflammatory cytokines such as interleukin (IL)-1β. These cytokines promote renal interstitial inflammation and promote sodium retention by tubular epithelial cells, thereby contributing to salt-sensitivity and hypertension. P2X7 receptors are also expressed in renal vascular endothelial cells, particularly in the pre-glomerular vasculature and vasa recta . ATP, released by endothelial cells, can activate endothelial P2X7 receptors in an autocrine/paracrine fashion to promote vasoconstriction, ultimately decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). Figure contains a modified illustration from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License ( https://creativecommons.org/licenses/by/4.0/ ).

    Techniques Used: Activation Assay, Filtration, Modification

    Validation of P2X7 deletion in P2rx7 −/− rats. ( A ) Partial decrease in P2rx7 mRNA abundance in the kidney of male P2rx7 −/− vs. WT using two PCR primer sets (n = 5 rats/group). ( B ) Trend for a partial decrease in P2rx7 mRNA abundance in the kidney of female P2rx7 −/− vs. WT (n = 4 rats/group). ( C ) Western blot demonstrating the absence of P2X7 protein expression in kidney samples of male and female P2rx7 −/− rats using an antibody directed against the C‐terminus of P2X7. GAPDH expression was used as a loading control (n = 3 rats/group). ( D ) Suppressed IL‐1β production by BMDM from male rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( E ) Suppressed IL‐1β production by BMDM from female rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( F ) Similar NO 2 − production by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 5–6 rats/group). ( G ) Similar induction of M1 polarisation marker genes by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 3 rats/group). Data are means ± SD and statistical analysis performed using t-test ( A , B ) or 2-way ANOVA with Holm–Sidak post hoc correction ( D – G ). For all analyses, P < 0.05 was considered significant.
    Figure Legend Snippet: Validation of P2X7 deletion in P2rx7 −/− rats. ( A ) Partial decrease in P2rx7 mRNA abundance in the kidney of male P2rx7 −/− vs. WT using two PCR primer sets (n = 5 rats/group). ( B ) Trend for a partial decrease in P2rx7 mRNA abundance in the kidney of female P2rx7 −/− vs. WT (n = 4 rats/group). ( C ) Western blot demonstrating the absence of P2X7 protein expression in kidney samples of male and female P2rx7 −/− rats using an antibody directed against the C‐terminus of P2X7. GAPDH expression was used as a loading control (n = 3 rats/group). ( D ) Suppressed IL‐1β production by BMDM from male rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( E ) Suppressed IL‐1β production by BMDM from female rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( F ) Similar NO 2 − production by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 5–6 rats/group). ( G ) Similar induction of M1 polarisation marker genes by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 3 rats/group). Data are means ± SD and statistical analysis performed using t-test ( A , B ) or 2-way ANOVA with Holm–Sidak post hoc correction ( D – G ). For all analyses, P < 0.05 was considered significant.

    Techniques Used: Western Blot, Expressing, Control, Marker

    Ex vivo renal artery contractility in male P2rx7 −/− rats. ( A ) Similar external K + -evoked constriction force in male WT and P2rx7 −/− rat renal artery. ( B ) Similar vasoconstriction of male WT and P2rx7 −/− rat renal arteries to increasing phenylephrine (PE) concentrations. ( C ) Impaired vasodilation of male P2rx7 −/− rat renal arteries to increasing acetylcholine (ACh) concentrations. ( D ) Similar vasodilation of male WT and P2rx7 −/− rat renal arteries to increasing sodium nitroprusside (SNP) concentrations. For all, n = 9–11 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A ) or 2-way ANOVA ( B – D ). For all analyses, P < 0.05 was considered significant.
    Figure Legend Snippet: Ex vivo renal artery contractility in male P2rx7 −/− rats. ( A ) Similar external K + -evoked constriction force in male WT and P2rx7 −/− rat renal artery. ( B ) Similar vasoconstriction of male WT and P2rx7 −/− rat renal arteries to increasing phenylephrine (PE) concentrations. ( C ) Impaired vasodilation of male P2rx7 −/− rat renal arteries to increasing acetylcholine (ACh) concentrations. ( D ) Similar vasodilation of male WT and P2rx7 −/− rat renal arteries to increasing sodium nitroprusside (SNP) concentrations. For all, n = 9–11 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A ) or 2-way ANOVA ( B – D ). For all analyses, P < 0.05 was considered significant.

    Techniques Used: Ex Vivo

    In vivo renal hemodynamics and the pressure natriuresis relationship in male P2rx7 −/− rats. ( A ) Change in mean arterial pressure (MAP) following ligation of coeliac, superior mesenteric, and distal aorta ligation. ( B ) Change in renal artery blood flow (RBF) as measured using a Transonic Doppler flow probe placed around the right main renal artery. ( C ) Change in renal vascular resistance (RVR). ( D ) Change in glomerular filtration rate (GFR). ( E ) Change in urinary sodium excretion rate (U Na V). ( F ) Change in urine flow rate (UV). ( G ) Urinary nitrite/nitrate excretion rate (U NOx V). For all, n = 9–10 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A – F ) or 2-way ANOVA with Holm–Sidak post hoc correction ( G ). For all analyses, P < 0.05 was considered significant.
    Figure Legend Snippet: In vivo renal hemodynamics and the pressure natriuresis relationship in male P2rx7 −/− rats. ( A ) Change in mean arterial pressure (MAP) following ligation of coeliac, superior mesenteric, and distal aorta ligation. ( B ) Change in renal artery blood flow (RBF) as measured using a Transonic Doppler flow probe placed around the right main renal artery. ( C ) Change in renal vascular resistance (RVR). ( D ) Change in glomerular filtration rate (GFR). ( E ) Change in urinary sodium excretion rate (U Na V). ( F ) Change in urine flow rate (UV). ( G ) Urinary nitrite/nitrate excretion rate (U NOx V). For all, n = 9–10 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A – F ) or 2-way ANOVA with Holm–Sidak post hoc correction ( G ). For all analyses, P < 0.05 was considered significant.

    Techniques Used: In Vivo, Ligation, Filtration

    Radiotelemetry blood pressure in healthy male P2rx7 −/− rats. Blood pressure was recorded for 5 consecutive days using radiotelemetry devices. Data from each 24 h period were averaged. ( A ) 24 h systolic and diastolic blood pressure profiles in WT and P2rx7 −/− rats. ( B ) Average systolic and diastolic blood pressure during light (inactive) and dark (active) 12 h phases in WT and P2rx7 −/− rats. n = 7–8 rats/group. Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction ( B ). For all analyses, P < 0.05 was considered significant.
    Figure Legend Snippet: Radiotelemetry blood pressure in healthy male P2rx7 −/− rats. Blood pressure was recorded for 5 consecutive days using radiotelemetry devices. Data from each 24 h period were averaged. ( A ) 24 h systolic and diastolic blood pressure profiles in WT and P2rx7 −/− rats. ( B ) Average systolic and diastolic blood pressure during light (inactive) and dark (active) 12 h phases in WT and P2rx7 −/− rats. n = 7–8 rats/group. Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction ( B ). For all analyses, P < 0.05 was considered significant.

    Techniques Used:

    Kidney injury, inflammation, and fibrosis in male P2rx7 −/− rats following chronic ANGII infusion. Male WT and P2rx7 −/− rats underwent 5–6 week ANGII infusion. Urine and kidneys were harvested at end of infusion for the quantification of kidney injury, inflammation and fibrosis. ( A ) Quantification of albuminuria following ANGII infusion (n = 4–7 rats/group). ( B ) Quantification of the tubular injury biomarker KIM-1 in urine following ANGII infusion (n = 5–8 rats/group). ( C ) Number of tubular casts in kidney sections stained with PAS (n = 6 rats/group). ( D ) Quantification of the macrophage marker CD68-positive area in kidney sections (n = 6 rats/group). ( E ) Quantification of perivascular collagen area in kidney sections (n = 6 rats/group). Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction to test for the effect of angiotensin II (ANGII), P2rx7 knockout (Genotype), and the interaction. For all analyses, P < 0.05 was considered significant.
    Figure Legend Snippet: Kidney injury, inflammation, and fibrosis in male P2rx7 −/− rats following chronic ANGII infusion. Male WT and P2rx7 −/− rats underwent 5–6 week ANGII infusion. Urine and kidneys were harvested at end of infusion for the quantification of kidney injury, inflammation and fibrosis. ( A ) Quantification of albuminuria following ANGII infusion (n = 4–7 rats/group). ( B ) Quantification of the tubular injury biomarker KIM-1 in urine following ANGII infusion (n = 5–8 rats/group). ( C ) Number of tubular casts in kidney sections stained with PAS (n = 6 rats/group). ( D ) Quantification of the macrophage marker CD68-positive area in kidney sections (n = 6 rats/group). ( E ) Quantification of perivascular collagen area in kidney sections (n = 6 rats/group). Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction to test for the effect of angiotensin II (ANGII), P2rx7 knockout (Genotype), and the interaction. For all analyses, P < 0.05 was considered significant.

    Techniques Used: Biomarker Assay, Staining, Marker, Knock-Out

    Related Articles

    Incubation:

    Article Title: Long non‑coding RNA BC168687 small interfering RNA reduces high glucose and high free fatty acid‑induced expression of P2X7 receptors in satellite glial cells.
    Article Snippet: .. The slides were washed in PBS and incubated with P2X7 primary antibody (cat no. APR-004-AO; 1:200; Alomone Labs, Jerusalem, Israel) overnight at 4 ̊C. ..

    Article Title: Characterization of 11 C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation.
    Article Snippet: .. Blocking was performed for 45 min in PBS with 5% BSA and 0.1% triton-X100, followed by P2X7 primary antibody (Alomone, APR008) incubation overnight at 4oC in PBS with 1% BSA and 0.1% triton at 1:200 dilution. ..

    Blocking Assay:

    Article Title: Characterization of 11 C-GSK1482160 for Targeting the P2X7 Receptor as a Biomarker for Neuroinflammation.
    Article Snippet: .. Blocking was performed for 45 min in PBS with 5% BSA and 0.1% triton-X100, followed by P2X7 primary antibody (Alomone, APR008) incubation overnight at 4oC in PBS with 1% BSA and 0.1% triton at 1:200 dilution. ..



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    ABclonal Biotechnology primary antibodies nlrp3, p2x7, pannexin-1, il-1β
    P2X7Rs modulate AMPA- and NMDA receptor-mediated excitatory neurotransmission in both an AP-dependent manner and AP-independent manner (A and B) Representative AMPA receptor-mediated sEPSC recordings from WT (left) and <t>P2X7R</t> deficient (right) mice at P21-28. (B, left) Cumulative distribution of the AMPA receptor-mediated sEPSCs frequency, summary of the frequency (B, middle), and amplitude (B, right) data showing that the frequency decreased while the amplitude was unchanged in P2X7R deficient mice compared to WT mice (Frequency wt: 1.68 ± 0.15 Hz, n = 10 vs. P2x7 −/− : 1.09 ± 0.09 Hz, n = 9; p = 0.005, unpaired t test: Amplitude wt: 17.06 ± 0.5 pA, n = 10 vs. P2x7 −/− :17.26 ± 0.59 pA, n = 9; p = 0.58, unpaired t test). (C) Summary of the frequency (left) and amplitude (right) from AMPA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice compared to WT mice (Frequency wt: 1.04 ± 0.09 Hz, n = 6 vs. P2x7 −/− : 0.61 ± 0.14 Hz, n = 8; p = 0.033, unpaired t test; Amplitude wt: 6.44 ± 0.45 pA, n = 10 vs. P2x7 −/− -: 5.98 ± 0.33 pA, n = 8; p = 0.89, unpaired t test). (D and E) Representative NMDA receptor-mediated sEPSC traces from WT (left) and P2X7R deficient (right) mice at P21-28. (E, left) Cumulative distribution of the NMDA receptor-mediated sEPSC frequency, summary of the frequency (E, middle), and amplitude (E, right) data displaying a decrease in frequency in P2X7R deficient mice in comparison with WT mice (Frequency wt: 0.66 ± 0.06 Hz, n = 7 vs. P2x7 −/− : 0.25 ± 0.02 Hz, n = 6; p = 0.001, unpaired t test; (Amplitude wt: 9.12 ± 1.36 pA, n = 7 vs. P2x7 −/− : 9.32 ± 0.96 pA, n = 6; p = 0.83, unpaired t test). (F) Summary of the frequency (left) and amplitude (right) from NMDA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice when compared to the WT counterparts (Frequency wt: 0.39 ± 0.027 Hz, n = 10 vs. P2x7 −/− : 0.19 ± 0.02 Hz, n = 11; p = 0.001, unpaired t test; Amplitude wt: 6.18 ± 0.66 pA, n = 10 vs. P2x7 −/− : 6.4 ± 0.6 pA, n = 11; p = 0.96, unpaired t test). The cumulative probability was assessed using the Kolmogorov-Smirnov test. Summary data are shown as the mean ± SEM. ∗ marks significant difference.
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    The role of P2X7 receptors in the hypertensive kidney. P2X7 receptors are non-selective cation channel receptors activated by extracellular adenosine triphosphate (ATP). P2X7 receptors are abundantly expressed by immune cells, such as macrophages. ATP released by damaged or activated cells activates P2X7 receptors on macrophages to mediate NOD−, LRR− and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and caspase-1 assembly leading to inflammasome activation, and the subsequent maturation and release of pro-inflammatory cytokines such as interleukin (IL)-1β. These cytokines promote renal interstitial inflammation and promote sodium retention by tubular epithelial cells, thereby contributing to salt-sensitivity and hypertension. P2X7 receptors are also expressed in renal vascular endothelial cells, particularly in the pre-glomerular vasculature and vasa recta . ATP, released by endothelial cells, can activate endothelial P2X7 receptors in an autocrine/paracrine fashion to promote vasoconstriction, ultimately decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). Figure contains a modified illustration from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License ( https://creativecommons.org/licenses/by/4.0/ ).

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: The role of P2X7 receptors in the hypertensive kidney. P2X7 receptors are non-selective cation channel receptors activated by extracellular adenosine triphosphate (ATP). P2X7 receptors are abundantly expressed by immune cells, such as macrophages. ATP released by damaged or activated cells activates P2X7 receptors on macrophages to mediate NOD−, LRR− and pyrin domain-containing protein 3 (NLRP3), Apoptosis-associated speck-like protein containing a caspase recruitment domain (CARD) (ASC) and caspase-1 assembly leading to inflammasome activation, and the subsequent maturation and release of pro-inflammatory cytokines such as interleukin (IL)-1β. These cytokines promote renal interstitial inflammation and promote sodium retention by tubular epithelial cells, thereby contributing to salt-sensitivity and hypertension. P2X7 receptors are also expressed in renal vascular endothelial cells, particularly in the pre-glomerular vasculature and vasa recta . ATP, released by endothelial cells, can activate endothelial P2X7 receptors in an autocrine/paracrine fashion to promote vasoconstriction, ultimately decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). Figure contains a modified illustration from Servier Medical Art. Servier Medical Art by Servier is licensed under a Creative Commons Attribution 4.0 Unported License ( https://creativecommons.org/licenses/by/4.0/ ).

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques: Activation Assay, Filtration, Modification

    Validation of P2X7 deletion in P2rx7 −/− rats. ( A ) Partial decrease in P2rx7 mRNA abundance in the kidney of male P2rx7 −/− vs. WT using two PCR primer sets (n = 5 rats/group). ( B ) Trend for a partial decrease in P2rx7 mRNA abundance in the kidney of female P2rx7 −/− vs. WT (n = 4 rats/group). ( C ) Western blot demonstrating the absence of P2X7 protein expression in kidney samples of male and female P2rx7 −/− rats using an antibody directed against the C‐terminus of P2X7. GAPDH expression was used as a loading control (n = 3 rats/group). ( D ) Suppressed IL‐1β production by BMDM from male rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( E ) Suppressed IL‐1β production by BMDM from female rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( F ) Similar NO 2 − production by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 5–6 rats/group). ( G ) Similar induction of M1 polarisation marker genes by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 3 rats/group). Data are means ± SD and statistical analysis performed using t-test ( A , B ) or 2-way ANOVA with Holm–Sidak post hoc correction ( D – G ). For all analyses, P < 0.05 was considered significant.

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: Validation of P2X7 deletion in P2rx7 −/− rats. ( A ) Partial decrease in P2rx7 mRNA abundance in the kidney of male P2rx7 −/− vs. WT using two PCR primer sets (n = 5 rats/group). ( B ) Trend for a partial decrease in P2rx7 mRNA abundance in the kidney of female P2rx7 −/− vs. WT (n = 4 rats/group). ( C ) Western blot demonstrating the absence of P2X7 protein expression in kidney samples of male and female P2rx7 −/− rats using an antibody directed against the C‐terminus of P2X7. GAPDH expression was used as a loading control (n = 3 rats/group). ( D ) Suppressed IL‐1β production by BMDM from male rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( E ) Suppressed IL‐1β production by BMDM from female rats primed for 4 h with 1 μg/mL of LPS, then stimulated for 1 h with 3 mM ATP (n = 5–6 rats/group). ( F ) Similar NO 2 − production by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 5–6 rats/group). ( G ) Similar induction of M1 polarisation marker genes by male WT and P2rx7 −/− BMDM following stimulation with LPS for 4 h (n = 3 rats/group). Data are means ± SD and statistical analysis performed using t-test ( A , B ) or 2-way ANOVA with Holm–Sidak post hoc correction ( D – G ). For all analyses, P < 0.05 was considered significant.

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques: Western Blot, Expressing, Control, Marker

    Ex vivo renal artery contractility in male P2rx7 −/− rats. ( A ) Similar external K + -evoked constriction force in male WT and P2rx7 −/− rat renal artery. ( B ) Similar vasoconstriction of male WT and P2rx7 −/− rat renal arteries to increasing phenylephrine (PE) concentrations. ( C ) Impaired vasodilation of male P2rx7 −/− rat renal arteries to increasing acetylcholine (ACh) concentrations. ( D ) Similar vasodilation of male WT and P2rx7 −/− rat renal arteries to increasing sodium nitroprusside (SNP) concentrations. For all, n = 9–11 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A ) or 2-way ANOVA ( B – D ). For all analyses, P < 0.05 was considered significant.

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: Ex vivo renal artery contractility in male P2rx7 −/− rats. ( A ) Similar external K + -evoked constriction force in male WT and P2rx7 −/− rat renal artery. ( B ) Similar vasoconstriction of male WT and P2rx7 −/− rat renal arteries to increasing phenylephrine (PE) concentrations. ( C ) Impaired vasodilation of male P2rx7 −/− rat renal arteries to increasing acetylcholine (ACh) concentrations. ( D ) Similar vasodilation of male WT and P2rx7 −/− rat renal arteries to increasing sodium nitroprusside (SNP) concentrations. For all, n = 9–11 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A ) or 2-way ANOVA ( B – D ). For all analyses, P < 0.05 was considered significant.

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques: Ex Vivo

    In vivo renal hemodynamics and the pressure natriuresis relationship in male P2rx7 −/− rats. ( A ) Change in mean arterial pressure (MAP) following ligation of coeliac, superior mesenteric, and distal aorta ligation. ( B ) Change in renal artery blood flow (RBF) as measured using a Transonic Doppler flow probe placed around the right main renal artery. ( C ) Change in renal vascular resistance (RVR). ( D ) Change in glomerular filtration rate (GFR). ( E ) Change in urinary sodium excretion rate (U Na V). ( F ) Change in urine flow rate (UV). ( G ) Urinary nitrite/nitrate excretion rate (U NOx V). For all, n = 9–10 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A – F ) or 2-way ANOVA with Holm–Sidak post hoc correction ( G ). For all analyses, P < 0.05 was considered significant.

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: In vivo renal hemodynamics and the pressure natriuresis relationship in male P2rx7 −/− rats. ( A ) Change in mean arterial pressure (MAP) following ligation of coeliac, superior mesenteric, and distal aorta ligation. ( B ) Change in renal artery blood flow (RBF) as measured using a Transonic Doppler flow probe placed around the right main renal artery. ( C ) Change in renal vascular resistance (RVR). ( D ) Change in glomerular filtration rate (GFR). ( E ) Change in urinary sodium excretion rate (U Na V). ( F ) Change in urine flow rate (UV). ( G ) Urinary nitrite/nitrate excretion rate (U NOx V). For all, n = 9–10 rats/group. Data are means ± SD and statistical analysis performed using t-test ( A – F ) or 2-way ANOVA with Holm–Sidak post hoc correction ( G ). For all analyses, P < 0.05 was considered significant.

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques: In Vivo, Ligation, Filtration

    Radiotelemetry blood pressure in healthy male P2rx7 −/− rats. Blood pressure was recorded for 5 consecutive days using radiotelemetry devices. Data from each 24 h period were averaged. ( A ) 24 h systolic and diastolic blood pressure profiles in WT and P2rx7 −/− rats. ( B ) Average systolic and diastolic blood pressure during light (inactive) and dark (active) 12 h phases in WT and P2rx7 −/− rats. n = 7–8 rats/group. Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction ( B ). For all analyses, P < 0.05 was considered significant.

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: Radiotelemetry blood pressure in healthy male P2rx7 −/− rats. Blood pressure was recorded for 5 consecutive days using radiotelemetry devices. Data from each 24 h period were averaged. ( A ) 24 h systolic and diastolic blood pressure profiles in WT and P2rx7 −/− rats. ( B ) Average systolic and diastolic blood pressure during light (inactive) and dark (active) 12 h phases in WT and P2rx7 −/− rats. n = 7–8 rats/group. Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction ( B ). For all analyses, P < 0.05 was considered significant.

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques:

    Kidney injury, inflammation, and fibrosis in male P2rx7 −/− rats following chronic ANGII infusion. Male WT and P2rx7 −/− rats underwent 5–6 week ANGII infusion. Urine and kidneys were harvested at end of infusion for the quantification of kidney injury, inflammation and fibrosis. ( A ) Quantification of albuminuria following ANGII infusion (n = 4–7 rats/group). ( B ) Quantification of the tubular injury biomarker KIM-1 in urine following ANGII infusion (n = 5–8 rats/group). ( C ) Number of tubular casts in kidney sections stained with PAS (n = 6 rats/group). ( D ) Quantification of the macrophage marker CD68-positive area in kidney sections (n = 6 rats/group). ( E ) Quantification of perivascular collagen area in kidney sections (n = 6 rats/group). Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction to test for the effect of angiotensin II (ANGII), P2rx7 knockout (Genotype), and the interaction. For all analyses, P < 0.05 was considered significant.

    Journal: Scientific Reports

    Article Title: P2X7 receptor knockout does not alter renal function or prevent angiotensin II-induced kidney injury in F344 rats

    doi: 10.1038/s41598-024-59635-x

    Figure Lengend Snippet: Kidney injury, inflammation, and fibrosis in male P2rx7 −/− rats following chronic ANGII infusion. Male WT and P2rx7 −/− rats underwent 5–6 week ANGII infusion. Urine and kidneys were harvested at end of infusion for the quantification of kidney injury, inflammation and fibrosis. ( A ) Quantification of albuminuria following ANGII infusion (n = 4–7 rats/group). ( B ) Quantification of the tubular injury biomarker KIM-1 in urine following ANGII infusion (n = 5–8 rats/group). ( C ) Number of tubular casts in kidney sections stained with PAS (n = 6 rats/group). ( D ) Quantification of the macrophage marker CD68-positive area in kidney sections (n = 6 rats/group). ( E ) Quantification of perivascular collagen area in kidney sections (n = 6 rats/group). Data are means ± SD and statistical analysis performed using 2-way ANOVA with Holm–Sidak post hoc correction to test for the effect of angiotensin II (ANGII), P2rx7 knockout (Genotype), and the interaction. For all analyses, P < 0.05 was considered significant.

    Article Snippet: Gel proteins were transferred to nitrocellulose membranes (Nitrocellulose/Filter Paper Sandwich, 0.2 μm, Invitrogen) and immunoblotted with the rabbit-anti-rat P2X7 primary antibody (APR-004, 1:500, Alomone Labs, Jerusalem, Israel) and mouse-anti-rat GAPDH (Ab8245, 1:1000, Abcam, Cambridge, UK) overnight.

    Techniques: Biomarker Assay, Staining, Marker, Knock-Out

    P2X7Rs modulate AMPA- and NMDA receptor-mediated excitatory neurotransmission in both an AP-dependent manner and AP-independent manner (A and B) Representative AMPA receptor-mediated sEPSC recordings from WT (left) and P2X7R deficient (right) mice at P21-28. (B, left) Cumulative distribution of the AMPA receptor-mediated sEPSCs frequency, summary of the frequency (B, middle), and amplitude (B, right) data showing that the frequency decreased while the amplitude was unchanged in P2X7R deficient mice compared to WT mice (Frequency wt: 1.68 ± 0.15 Hz, n = 10 vs. P2x7 −/− : 1.09 ± 0.09 Hz, n = 9; p = 0.005, unpaired t test: Amplitude wt: 17.06 ± 0.5 pA, n = 10 vs. P2x7 −/− :17.26 ± 0.59 pA, n = 9; p = 0.58, unpaired t test). (C) Summary of the frequency (left) and amplitude (right) from AMPA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice compared to WT mice (Frequency wt: 1.04 ± 0.09 Hz, n = 6 vs. P2x7 −/− : 0.61 ± 0.14 Hz, n = 8; p = 0.033, unpaired t test; Amplitude wt: 6.44 ± 0.45 pA, n = 10 vs. P2x7 −/− -: 5.98 ± 0.33 pA, n = 8; p = 0.89, unpaired t test). (D and E) Representative NMDA receptor-mediated sEPSC traces from WT (left) and P2X7R deficient (right) mice at P21-28. (E, left) Cumulative distribution of the NMDA receptor-mediated sEPSC frequency, summary of the frequency (E, middle), and amplitude (E, right) data displaying a decrease in frequency in P2X7R deficient mice in comparison with WT mice (Frequency wt: 0.66 ± 0.06 Hz, n = 7 vs. P2x7 −/− : 0.25 ± 0.02 Hz, n = 6; p = 0.001, unpaired t test; (Amplitude wt: 9.12 ± 1.36 pA, n = 7 vs. P2x7 −/− : 9.32 ± 0.96 pA, n = 6; p = 0.83, unpaired t test). (F) Summary of the frequency (left) and amplitude (right) from NMDA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice when compared to the WT counterparts (Frequency wt: 0.39 ± 0.027 Hz, n = 10 vs. P2x7 −/− : 0.19 ± 0.02 Hz, n = 11; p = 0.001, unpaired t test; Amplitude wt: 6.18 ± 0.66 pA, n = 10 vs. P2x7 −/− : 6.4 ± 0.6 pA, n = 11; p = 0.96, unpaired t test). The cumulative probability was assessed using the Kolmogorov-Smirnov test. Summary data are shown as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: P2X7Rs modulate AMPA- and NMDA receptor-mediated excitatory neurotransmission in both an AP-dependent manner and AP-independent manner (A and B) Representative AMPA receptor-mediated sEPSC recordings from WT (left) and P2X7R deficient (right) mice at P21-28. (B, left) Cumulative distribution of the AMPA receptor-mediated sEPSCs frequency, summary of the frequency (B, middle), and amplitude (B, right) data showing that the frequency decreased while the amplitude was unchanged in P2X7R deficient mice compared to WT mice (Frequency wt: 1.68 ± 0.15 Hz, n = 10 vs. P2x7 −/− : 1.09 ± 0.09 Hz, n = 9; p = 0.005, unpaired t test: Amplitude wt: 17.06 ± 0.5 pA, n = 10 vs. P2x7 −/− :17.26 ± 0.59 pA, n = 9; p = 0.58, unpaired t test). (C) Summary of the frequency (left) and amplitude (right) from AMPA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice compared to WT mice (Frequency wt: 1.04 ± 0.09 Hz, n = 6 vs. P2x7 −/− : 0.61 ± 0.14 Hz, n = 8; p = 0.033, unpaired t test; Amplitude wt: 6.44 ± 0.45 pA, n = 10 vs. P2x7 −/− -: 5.98 ± 0.33 pA, n = 8; p = 0.89, unpaired t test). (D and E) Representative NMDA receptor-mediated sEPSC traces from WT (left) and P2X7R deficient (right) mice at P21-28. (E, left) Cumulative distribution of the NMDA receptor-mediated sEPSC frequency, summary of the frequency (E, middle), and amplitude (E, right) data displaying a decrease in frequency in P2X7R deficient mice in comparison with WT mice (Frequency wt: 0.66 ± 0.06 Hz, n = 7 vs. P2x7 −/− : 0.25 ± 0.02 Hz, n = 6; p = 0.001, unpaired t test; (Amplitude wt: 9.12 ± 1.36 pA, n = 7 vs. P2x7 −/− : 9.32 ± 0.96 pA, n = 6; p = 0.83, unpaired t test). (F) Summary of the frequency (left) and amplitude (right) from NMDA receptor-mediated mEPSCs showing the decrease in frequency in P2X7R deficient mice when compared to the WT counterparts (Frequency wt: 0.39 ± 0.027 Hz, n = 10 vs. P2x7 −/− : 0.19 ± 0.02 Hz, n = 11; p = 0.001, unpaired t test; Amplitude wt: 6.18 ± 0.66 pA, n = 10 vs. P2x7 −/− : 6.4 ± 0.6 pA, n = 11; p = 0.96, unpaired t test). The cumulative probability was assessed using the Kolmogorov-Smirnov test. Summary data are shown as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques: Comparison

    Pharmacological manipulation of P2X7Rs modulates NMDA receptor-mediated excitatory neurotransmission in both an AP-dependent manner and AP-independent manner (A) Schematic of the experimental setup. (B–D) Representative sEPSC traces before (upper two), during (middle two), and after BzATP application (lower two). (C, right) Cumulative probability of sEPSCs interevent intervals and (C, middle and left) normalized frequencies and amplitudes before, during, and after BzATP application. BzATP application increased the number of events but not the amplitude (Normalized frequency (%): baseline: 99.9 ± 15.22; BzATP: 363.39 ± 47.52; Washout: 92.39 ± 28.27; n = 6; baseline vs. BzATP, p < 0.001, one-way ANOVA repeated measures by Dunnett’s test). (D, right) Cumulative probability of sEPSCs interevent intervals and (D, left) normalized frequencies and amplitudes before, during, and after BzATP application in the presence of the selective P2X7R antagonist JNJ-47965567. The increase in frequency was reversed by inhibition of P2X7Rs (Normalized frequency (%): baseline: 94.32 ± 6.83; BzATP: 106.71 ± 12.44; Washout: 108.22 ± 18.11; n = 9; baseline vs. BzATP, p = 0.73, one-way ANOVA repeated measures by Dunnett’s test). (E and F) BzATP increased the frequency of NMDA receptor-mediated mEPSCs (Normalized frequency (%): baseline: 100 ± 9.95; BzATP: 368.99 ± 57.94; Washout: 109.39 ± 10.02; n = 6; baseline vs. BzATP, p = 0.01, one-way ANOVA repeated measures by Dunnett’s test), and (F) this increase was inhibited in the presence of JNJ-47965567 P2X7Rs (Normalized frequency (%): baseline: 100 ± 10.06; BzATP: 97.33 ± 9.99; Washout: 82.89 ± 8.57; n = 7; baseline vs. BzATP, p = 0.73, one-way ANOVA repeated measures by Dunnett’s test). (G) P2X4R protein expression from mouse hippocampi lysates from WT and P2X7R-deficient animals were determined by immunoblotting. Graphs show the densitometric evaluation (n = 6; unpaired t test). The whole blot instead of bands was cropped, since the cropped part held no value (no signal or anything is shown on the rest). All protein bands are shown on the cropped Western blot. (H) NMDARs-sEPSC in the presence of P2X4R selective antagonist 5-BDBD in P2X7R deficient mice. 5-BDBD application reverted the BzATP-induced frequency potentiation (baseline: 0.245 ± 0.02, BzATP: 0.257 ± 0.024, Washout: 0.24 ± 0.03, baseline vs. BzATP, p = 0.92, one-way ANOVA repeated measures by Dunnett’s test). The Kolmogorov-Smirnov test was used to test the significance of cumulative probability. The normalized frequencies and amplitudes are displayed as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: Pharmacological manipulation of P2X7Rs modulates NMDA receptor-mediated excitatory neurotransmission in both an AP-dependent manner and AP-independent manner (A) Schematic of the experimental setup. (B–D) Representative sEPSC traces before (upper two), during (middle two), and after BzATP application (lower two). (C, right) Cumulative probability of sEPSCs interevent intervals and (C, middle and left) normalized frequencies and amplitudes before, during, and after BzATP application. BzATP application increased the number of events but not the amplitude (Normalized frequency (%): baseline: 99.9 ± 15.22; BzATP: 363.39 ± 47.52; Washout: 92.39 ± 28.27; n = 6; baseline vs. BzATP, p < 0.001, one-way ANOVA repeated measures by Dunnett’s test). (D, right) Cumulative probability of sEPSCs interevent intervals and (D, left) normalized frequencies and amplitudes before, during, and after BzATP application in the presence of the selective P2X7R antagonist JNJ-47965567. The increase in frequency was reversed by inhibition of P2X7Rs (Normalized frequency (%): baseline: 94.32 ± 6.83; BzATP: 106.71 ± 12.44; Washout: 108.22 ± 18.11; n = 9; baseline vs. BzATP, p = 0.73, one-way ANOVA repeated measures by Dunnett’s test). (E and F) BzATP increased the frequency of NMDA receptor-mediated mEPSCs (Normalized frequency (%): baseline: 100 ± 9.95; BzATP: 368.99 ± 57.94; Washout: 109.39 ± 10.02; n = 6; baseline vs. BzATP, p = 0.01, one-way ANOVA repeated measures by Dunnett’s test), and (F) this increase was inhibited in the presence of JNJ-47965567 P2X7Rs (Normalized frequency (%): baseline: 100 ± 10.06; BzATP: 97.33 ± 9.99; Washout: 82.89 ± 8.57; n = 7; baseline vs. BzATP, p = 0.73, one-way ANOVA repeated measures by Dunnett’s test). (G) P2X4R protein expression from mouse hippocampi lysates from WT and P2X7R-deficient animals were determined by immunoblotting. Graphs show the densitometric evaluation (n = 6; unpaired t test). The whole blot instead of bands was cropped, since the cropped part held no value (no signal or anything is shown on the rest). All protein bands are shown on the cropped Western blot. (H) NMDARs-sEPSC in the presence of P2X4R selective antagonist 5-BDBD in P2X7R deficient mice. 5-BDBD application reverted the BzATP-induced frequency potentiation (baseline: 0.245 ± 0.02, BzATP: 0.257 ± 0.024, Washout: 0.24 ± 0.03, baseline vs. BzATP, p = 0.92, one-way ANOVA repeated measures by Dunnett’s test). The Kolmogorov-Smirnov test was used to test the significance of cumulative probability. The normalized frequencies and amplitudes are displayed as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques: Inhibition, Expressing, Western Blot

    P2X7Rs affect excitatory neurotransmission through the EC-GC pathway but not MC-GC pathway (A) Stimulation pattern showing the position of the stimulating and recording electrodes. (B) The representative traces before, during, and after BzATP application in the presence of 1.3 mM Ca2+/2 Mm Mg2+. (C and D) The 1st stimulus-induced current amplitude changed cross time. DCG-IV perfusion significantly decreased the current amplitude. (D, left) BzATP alone significantly decreased the PPR (PPR: baseline: 2.00 ± 0.09; BzATP: 1.75 ± 0.07; Washout: 2.16 ± 0.23; n = 6; baseline vs. BzATP, p = 0.0249, one-way ANOVA repeated measures by Dunnett’s test). (D, middle) BzATP-induced PPR elevation was inhibited by JNJ-4796567 (PPR: baseline: 1.75 ± 0.15; BzATP: 1.75 ± 0.0.08; Washout: 1.85 ± 0.16; n = 7; baseline vs. BzATP p = 0.99, one-way ANOVA repeated measures by Dunnett’s test). (D, right) BzATP-induced PPR change was also inhibited by another P2X7Rs antagonist A 438079 (PPR: baseline: 1.82 ± 0.08; BzATP: 1.72 ± 0.05; Washout: 1.72 ± 0.08; n = 6; baseline vs. BzATP p = 0.44, one-way ANOVA repeated measures by Dunnett’s test). (E) The BzATP-induced reduction of PPR also showed in MPP (PPR: baseline: 1.56 ± 0.05; BzATP: 1.36 ± 0.02; Washout: 1.47 ± 0.04; n = 6; baseline vs. BzATP p = 0.02, one-way ANOVA repeated measures by Dunnett’s test). (F) Stimulation pattern for the MC-GC pathway. (G) The representative traces before, during and after BzATP application in the presence of 1.3 mM Ca2+/2 Mm Mg2+. (H) BzATP application and DCG-IV administration did not change 1st stimulus-induced current amplitude. (I) BzATP application did not alter PPR in the MC-GC pathway (PPR: baseline: 1.98 ± 0.09; BzATP: 1.96 ± 0.07; Washout: 2.00 ± 0.12; n = 6; baseline vs. BzATP, p = 0.56, one-way ANOVA repeated measures by Dunnett’s test). (J) Two representative DG GCs from WT and P2X7R deficient mice (objective: 20x; scale bar: 50 μm). (K–N) Dendritic morphology of DG GCs. The number of intersections, dendritic length, Area cell body and number of endings were not different between P2X7R deficient mice and WT mice (mean length (μm): wt: 756.57 ± 68.56, n = 13 vs. P2x7−/−:792.64 ± 62.71, n = 13, p = 0.92, unpaired t test; Area Cell Body (μm 2 ): wt: 122.83 ± 7.99, n = 13 vs. P2x7−/−: 134.84 ± 1.00, n = 13, p = 0.23, unpaired t test; Number of Endings: wt: 16.38 ± 0.65, n = 13 vs. P2x7−/−: 14.38 ± 1.05, n = 13, p = 0.6, unpaired t test). (O) Two dendritic branches from 150 μm segment (objective: 60x; scale bar: 10 μm). (P) Quantification of the spine number per μm was not significantly different between mice of the two genotypes (n = 13–17). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: P2X7Rs affect excitatory neurotransmission through the EC-GC pathway but not MC-GC pathway (A) Stimulation pattern showing the position of the stimulating and recording electrodes. (B) The representative traces before, during, and after BzATP application in the presence of 1.3 mM Ca2+/2 Mm Mg2+. (C and D) The 1st stimulus-induced current amplitude changed cross time. DCG-IV perfusion significantly decreased the current amplitude. (D, left) BzATP alone significantly decreased the PPR (PPR: baseline: 2.00 ± 0.09; BzATP: 1.75 ± 0.07; Washout: 2.16 ± 0.23; n = 6; baseline vs. BzATP, p = 0.0249, one-way ANOVA repeated measures by Dunnett’s test). (D, middle) BzATP-induced PPR elevation was inhibited by JNJ-4796567 (PPR: baseline: 1.75 ± 0.15; BzATP: 1.75 ± 0.0.08; Washout: 1.85 ± 0.16; n = 7; baseline vs. BzATP p = 0.99, one-way ANOVA repeated measures by Dunnett’s test). (D, right) BzATP-induced PPR change was also inhibited by another P2X7Rs antagonist A 438079 (PPR: baseline: 1.82 ± 0.08; BzATP: 1.72 ± 0.05; Washout: 1.72 ± 0.08; n = 6; baseline vs. BzATP p = 0.44, one-way ANOVA repeated measures by Dunnett’s test). (E) The BzATP-induced reduction of PPR also showed in MPP (PPR: baseline: 1.56 ± 0.05; BzATP: 1.36 ± 0.02; Washout: 1.47 ± 0.04; n = 6; baseline vs. BzATP p = 0.02, one-way ANOVA repeated measures by Dunnett’s test). (F) Stimulation pattern for the MC-GC pathway. (G) The representative traces before, during and after BzATP application in the presence of 1.3 mM Ca2+/2 Mm Mg2+. (H) BzATP application and DCG-IV administration did not change 1st stimulus-induced current amplitude. (I) BzATP application did not alter PPR in the MC-GC pathway (PPR: baseline: 1.98 ± 0.09; BzATP: 1.96 ± 0.07; Washout: 2.00 ± 0.12; n = 6; baseline vs. BzATP, p = 0.56, one-way ANOVA repeated measures by Dunnett’s test). (J) Two representative DG GCs from WT and P2X7R deficient mice (objective: 20x; scale bar: 50 μm). (K–N) Dendritic morphology of DG GCs. The number of intersections, dendritic length, Area cell body and number of endings were not different between P2X7R deficient mice and WT mice (mean length (μm): wt: 756.57 ± 68.56, n = 13 vs. P2x7−/−:792.64 ± 62.71, n = 13, p = 0.92, unpaired t test; Area Cell Body (μm 2 ): wt: 122.83 ± 7.99, n = 13 vs. P2x7−/−: 134.84 ± 1.00, n = 13, p = 0.23, unpaired t test; Number of Endings: wt: 16.38 ± 0.65, n = 13 vs. P2x7−/−: 14.38 ± 1.05, n = 13, p = 0.6, unpaired t test). (O) Two dendritic branches from 150 μm segment (objective: 60x; scale bar: 10 μm). (P) Quantification of the spine number per μm was not significantly different between mice of the two genotypes (n = 13–17). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques:

    P2X7Rs regulate EC-GC axonal boutons calcium influx (A) The scheme for virus injection. (B, upper) Location of virus injection in the LEC (objective: 4X; scale bar: 200 μm). (B, lower) Virus expression in LPP and MPP (objective: 2X; scale bar: 50 μm). (C) Co-staining GCaMP6s infected fibers with presynaptic marker VGlut1 and postsynaptic marker Homer1 (objective: 60X oil; scale bar: 1 μm). VGlut1 but not Homer1 localized in the GCaMP6s infected axonal boutons. (D) P2X7R immunostaining in WT and P2X7R deficient mice (objective: 60X oil; scale bar: 20 μm and 1 μm). Deconvoluted image showing P2X7R puncta (red dots) on LPP boutons (green) in WT but not in P2X7R deficient mice. The localization of P2X7R puncta on boutons (indicated by arrows) in the XY (big square), YZ (rectangle on the right), and XZ (rectangle on the left) dimensions (objective: 60X oil; scale bar: 5 μm). (E) Schematic of the method used for calcium imaging under a multiphoton microscope. (F) LPP-boutons calcium imaging in the presence of 1.3 mM Ca2+/2 mM Mg2+. Representative boutons calcium traces for one slice (upper) and the average traces from 8 slices (middle). The lower summarized table showed that BzATP application elevated the calcium influx peak amplitude (BL(%DF/F0): 16.75 ± 1.45 VS. BzATP (%DF/F0):19.45 ± 1.24, n = 8; paired t test, p = 0.002) and slightly increased the area under the curve (BL(A.U): 979.86 ± 96.25 VS. BzATP (A.U):1103.85 ± 92.83, n = 8; paired t test, p = 0.062). (G) JNJ-4795567 perfusion inhibited the elevation induced by BzATP (BL(%DF/F0): 26.44 ± 2.14 VS BzATP (%DF/F0):25.35 ± 2.35, n = 7, paired t test, p = 0.15) (BL(A.U): 1383.42 ± 151.24 VS BzATP (A.U):1347.2 ± 164.98, n = 7; paired t test, p = 0.56). (H) MPP-boutons calcium imaging in the presence of 1.3 mM Ca2+/2 mM Mg2+. BzATP application also increased the calcium influx peak amplitude (BL(%DF/F0): 14.28 ± 1.98 VS. BzATP (%DF/F0):17.08 ± 1.03, n = 6, paired t test, p = 0.04) and area under the curve (BL(A.U): 843.8 ± 54.17 VS. BzATP (A.U):1048 ± 123.5, n = 6; paired t test, p = 0.078). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: P2X7Rs regulate EC-GC axonal boutons calcium influx (A) The scheme for virus injection. (B, upper) Location of virus injection in the LEC (objective: 4X; scale bar: 200 μm). (B, lower) Virus expression in LPP and MPP (objective: 2X; scale bar: 50 μm). (C) Co-staining GCaMP6s infected fibers with presynaptic marker VGlut1 and postsynaptic marker Homer1 (objective: 60X oil; scale bar: 1 μm). VGlut1 but not Homer1 localized in the GCaMP6s infected axonal boutons. (D) P2X7R immunostaining in WT and P2X7R deficient mice (objective: 60X oil; scale bar: 20 μm and 1 μm). Deconvoluted image showing P2X7R puncta (red dots) on LPP boutons (green) in WT but not in P2X7R deficient mice. The localization of P2X7R puncta on boutons (indicated by arrows) in the XY (big square), YZ (rectangle on the right), and XZ (rectangle on the left) dimensions (objective: 60X oil; scale bar: 5 μm). (E) Schematic of the method used for calcium imaging under a multiphoton microscope. (F) LPP-boutons calcium imaging in the presence of 1.3 mM Ca2+/2 mM Mg2+. Representative boutons calcium traces for one slice (upper) and the average traces from 8 slices (middle). The lower summarized table showed that BzATP application elevated the calcium influx peak amplitude (BL(%DF/F0): 16.75 ± 1.45 VS. BzATP (%DF/F0):19.45 ± 1.24, n = 8; paired t test, p = 0.002) and slightly increased the area under the curve (BL(A.U): 979.86 ± 96.25 VS. BzATP (A.U):1103.85 ± 92.83, n = 8; paired t test, p = 0.062). (G) JNJ-4795567 perfusion inhibited the elevation induced by BzATP (BL(%DF/F0): 26.44 ± 2.14 VS BzATP (%DF/F0):25.35 ± 2.35, n = 7, paired t test, p = 0.15) (BL(A.U): 1383.42 ± 151.24 VS BzATP (A.U):1347.2 ± 164.98, n = 7; paired t test, p = 0.56). (H) MPP-boutons calcium imaging in the presence of 1.3 mM Ca2+/2 mM Mg2+. BzATP application also increased the calcium influx peak amplitude (BL(%DF/F0): 14.28 ± 1.98 VS. BzATP (%DF/F0):17.08 ± 1.03, n = 6, paired t test, p = 0.04) and area under the curve (BL(A.U): 843.8 ± 54.17 VS. BzATP (A.U):1048 ± 123.5, n = 6; paired t test, p = 0.078). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques: Virus, Injection, Expressing, Staining, Infection, Marker, Immunostaining, Imaging, Microscopy

    P2X7Rs deficiency alleviate schizophrenia-like behavior and restore EC-GC synapse alteration in juvenile (A) Schematic of the experiment. (B) Locomotor activity in T maze. PCP treated animals moved longer distance in comparison with saline treated group in WT, but both PCP and saline treated animals did not show any difference in P2X7R deficient groups (wt-saline: 1967 ± 155.8 cm, n = 9 vs. wt-PCP: 2623 ± 241.14 cm, n = 7, p = 0.047; P2x7 −/− -saline: 2134 ± 183.6 cm, n = 8 vs. P2x7 −/− -PCP: 2038 ± 158.5 cm, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). (C) Spontaneous alteration in T maze. PCP injection in WT showed less successful alteration compared the saline group (wt-saline: 61.71 ± 2.79%, n = 9 vs. wt-PCP: 49.20 ± 7.10%, n = 7, p = 0.02; P2x7 −/− -saline: 61.88 ± 2.82%, n = 8 vs. P2x7 −/− -PCP: 61.52 ± 3.59%, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). No change has been observed in the P2X7R deficient mice injected with PCP or saline. (D) The novel object recognition test. PCP treatment did not show any recognition preference (wt-saline: 59.61 ± 6.74%, n = 9 vs. wt-PCP: 63.25 ± 10.41%, n = 7, p > 0.99; P2x7 −/− -saline: 61.47 ± 8.89%, n = 8 vs. P2x7 −/− -PCP: 62.57 ± 9.40%, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). (E) The scheme for electrophysiological recordings. (F) The representative traces for AMPA/NMDA ratio under different conditions. (G) The AMPA/NMDA ratio in WT and P2X7R deficient mice treated with either PCP or saline. The AMPA/NMDA ratio was determined by calculating the AMPA current amplitude relative to NMDARs current amplitude at 50 m post-stimulus. PCP-treated mice showed a significantly higher AMPA/NMDA ratio than saline-treated mice in WT but not in P2X7R deficient (wt-saline: 1.31 ± 0.17, n = 12 vs. wt-PCP: 3.00 ± 0.33, n = 13, p < 0.0001; P2x7 −/− -saline: 1.62 ± 0.25, n = 10 vs. P2x7 −/− -PCP: 1.85 ± 0.16, n = 17, p = 0.95, one-way ANOVA by Dunnett’s test). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: P2X7Rs deficiency alleviate schizophrenia-like behavior and restore EC-GC synapse alteration in juvenile (A) Schematic of the experiment. (B) Locomotor activity in T maze. PCP treated animals moved longer distance in comparison with saline treated group in WT, but both PCP and saline treated animals did not show any difference in P2X7R deficient groups (wt-saline: 1967 ± 155.8 cm, n = 9 vs. wt-PCP: 2623 ± 241.14 cm, n = 7, p = 0.047; P2x7 −/− -saline: 2134 ± 183.6 cm, n = 8 vs. P2x7 −/− -PCP: 2038 ± 158.5 cm, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). (C) Spontaneous alteration in T maze. PCP injection in WT showed less successful alteration compared the saline group (wt-saline: 61.71 ± 2.79%, n = 9 vs. wt-PCP: 49.20 ± 7.10%, n = 7, p = 0.02; P2x7 −/− -saline: 61.88 ± 2.82%, n = 8 vs. P2x7 −/− -PCP: 61.52 ± 3.59%, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). No change has been observed in the P2X7R deficient mice injected with PCP or saline. (D) The novel object recognition test. PCP treatment did not show any recognition preference (wt-saline: 59.61 ± 6.74%, n = 9 vs. wt-PCP: 63.25 ± 10.41%, n = 7, p > 0.99; P2x7 −/− -saline: 61.47 ± 8.89%, n = 8 vs. P2x7 −/− -PCP: 62.57 ± 9.40%, n = 8, p > 0.99, one-way ANOVA by Dunnett’s test). (E) The scheme for electrophysiological recordings. (F) The representative traces for AMPA/NMDA ratio under different conditions. (G) The AMPA/NMDA ratio in WT and P2X7R deficient mice treated with either PCP or saline. The AMPA/NMDA ratio was determined by calculating the AMPA current amplitude relative to NMDARs current amplitude at 50 m post-stimulus. PCP-treated mice showed a significantly higher AMPA/NMDA ratio than saline-treated mice in WT but not in P2X7R deficient (wt-saline: 1.31 ± 0.17, n = 12 vs. wt-PCP: 3.00 ± 0.33, n = 13, p < 0.0001; P2x7 −/− -saline: 1.62 ± 0.25, n = 10 vs. P2x7 −/− -PCP: 1.85 ± 0.16, n = 17, p = 0.95, one-way ANOVA by Dunnett’s test). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques: Activity Assay, Comparison, Saline, Injection

    P2X7Rs deficiency alleviates schizophrenia-like behavior in adult (A) Scheme of the experiment. (B) Locomotor activity in the open field test. PCP-treated mice traveled a longer distance than saline-treated mice. However, the locomotor hyperactivity induced by PCP was significantly alleviated in the P2X7R deficient group (wt-saline: 4024 ± 106.70 cm, n = 15 vs. wt-PCP: 4662.50 ± 129.22 cm, n = 12, p = 0.035; P2x7 −/− -saline: 4007.68 ± 185.78 cm, n = 9 vs. P2x7 −/− -PCP: 4126.31 ± 149.16 cm, n = 12, p = 0.99, one-way ANOVA by Dunnett’s test). (C) Spontaneous activity test in T maze. PCP treatment group did not show a significant difference in both tests (wt-saline: 51.47 ± 1.99%, n = 15 vs. wt-PCP: 51.66 ± 2.41%, n = 12, p = 0.81; P2x7 −/− -saline: 57.04 ± 3.88%, n = 9 vs. P2x7 −/− -PCP: 57.69 ± 1.97%, n = 12, p = 0.79, one-way ANOVA by Dunnett’s test). (D) The novel object recognition in T maze. No difference was observed in different groups (wt-saline: 68.84 ± 2.81%, n = 15 vs. wt-PCP: 62.96 ± 3.34%, n = 12, p = 0.81; P2x7 −/− -saline: 65.66 ± 6.25%, n = 9 vs. P2x7 −/− -PCP: 66.56 ± 4.38%, n = 12, p = 0.79, one-way ANOVA by Dunnett’s test). (E) The scheme of the social preference test and no difference has been observed from 4 groups (wt-saline: 72.30 ± 3.22%, n = 15 vs. wt-PCP: 71.53 ± 2.61%, n = 12, p = 0.89; P2x7 −/− -saline: 64.27 ± 3.47%, n = 9 vs. P2x7 −/− -PCP: 74.91 ± 2.24%, n = 12, p = 0.13, one-way ANOVA by Dunnett’s test). (F) The acoustic startle setup. (F, middle) The PCP-treated group displayed a decrease in PPI, which was restored in the P2X7R deficient group (wt-saline: 51.55 ± 4.07%, n = 15, vs. wt-PCP: 28.09 ± 3.95%, n = 12, p = 0.001; P2x7 −/− -saline: 44.69 ± 8.19%, n = 9 vs. P2x7 −/− -PCP: 42.20 ± 3.12%, n = 12, p = 0.99, two-way ANOVA by Dunnett’s test). (F, right) The startle reflex in response to 80, 90, 100, 110, and 120 dB. Compared to WT, P2X7R deficient mice showed less response to 120 dB (P120: wt-saline: 266.27 ± 14,60 mV, n = 15 vs. P2x7 −/− -saline: 134.39 ± 20.44 mV, n = 9, p = 0.009, two-way ANOVA by Dunnett’s test). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Journal: iScience

    Article Title: P2X7 purinergic receptor modulates dentate gyrus excitatory neurotransmission and alleviates schizophrenia-like symptoms in mouse

    doi: 10.1016/j.isci.2023.107560

    Figure Lengend Snippet: P2X7Rs deficiency alleviates schizophrenia-like behavior in adult (A) Scheme of the experiment. (B) Locomotor activity in the open field test. PCP-treated mice traveled a longer distance than saline-treated mice. However, the locomotor hyperactivity induced by PCP was significantly alleviated in the P2X7R deficient group (wt-saline: 4024 ± 106.70 cm, n = 15 vs. wt-PCP: 4662.50 ± 129.22 cm, n = 12, p = 0.035; P2x7 −/− -saline: 4007.68 ± 185.78 cm, n = 9 vs. P2x7 −/− -PCP: 4126.31 ± 149.16 cm, n = 12, p = 0.99, one-way ANOVA by Dunnett’s test). (C) Spontaneous activity test in T maze. PCP treatment group did not show a significant difference in both tests (wt-saline: 51.47 ± 1.99%, n = 15 vs. wt-PCP: 51.66 ± 2.41%, n = 12, p = 0.81; P2x7 −/− -saline: 57.04 ± 3.88%, n = 9 vs. P2x7 −/− -PCP: 57.69 ± 1.97%, n = 12, p = 0.79, one-way ANOVA by Dunnett’s test). (D) The novel object recognition in T maze. No difference was observed in different groups (wt-saline: 68.84 ± 2.81%, n = 15 vs. wt-PCP: 62.96 ± 3.34%, n = 12, p = 0.81; P2x7 −/− -saline: 65.66 ± 6.25%, n = 9 vs. P2x7 −/− -PCP: 66.56 ± 4.38%, n = 12, p = 0.79, one-way ANOVA by Dunnett’s test). (E) The scheme of the social preference test and no difference has been observed from 4 groups (wt-saline: 72.30 ± 3.22%, n = 15 vs. wt-PCP: 71.53 ± 2.61%, n = 12, p = 0.89; P2x7 −/− -saline: 64.27 ± 3.47%, n = 9 vs. P2x7 −/− -PCP: 74.91 ± 2.24%, n = 12, p = 0.13, one-way ANOVA by Dunnett’s test). (F) The acoustic startle setup. (F, middle) The PCP-treated group displayed a decrease in PPI, which was restored in the P2X7R deficient group (wt-saline: 51.55 ± 4.07%, n = 15, vs. wt-PCP: 28.09 ± 3.95%, n = 12, p = 0.001; P2x7 −/− -saline: 44.69 ± 8.19%, n = 9 vs. P2x7 −/− -PCP: 42.20 ± 3.12%, n = 12, p = 0.99, two-way ANOVA by Dunnett’s test). (F, right) The startle reflex in response to 80, 90, 100, 110, and 120 dB. Compared to WT, P2X7R deficient mice showed less response to 120 dB (P120: wt-saline: 266.27 ± 14,60 mV, n = 15 vs. P2x7 −/− -saline: 134.39 ± 20.44 mV, n = 9, p = 0.009, two-way ANOVA by Dunnett’s test). The data are presented as the mean ± SEM. ∗ marks significant difference.

    Article Snippet: A rabbit anti-P2X7R primary antibody (APR-004, Alomone Labs, Israel) was diluted 1:100 in blocking buffer, and a chicken anti-GFP primary antibody (GFP-1020, Aves Labs, CA) was diluted 1:1000 in blocking buffer.

    Techniques: Activity Assay, Saline