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Tocris cgrp 8 37
Cgrp 8 37, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 33 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cgrp+8%E2%80%9337+%28rat%29/pmc12032830-1048-0-3?v=Tocris
Average 93 stars, based on 33 article reviews

cgrp 8 37 - by Bioz Stars, 2026-07

93/100 stars

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Journal: Developmental cell

Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice

doi: 10.1016/j.devcel.2024.05.019

Figure Lengend Snippet: (A) Diagram of experimental design and representative images from shaved TRPV1 activated mice and controls. Mice monitored for hair coat growth for 12 days after the last TRPV1 activation with CNO (postnatal day 63). (B) Enlarged dashed rectangle from panel A depicting hair growth in a TRPV1 activated mouse. (C) HF length quantification of dorsal skin from mice treated as in A. Data combined from 6 to 8 HF per mouse, taken from 6 mice per group (****p<0.0001). (D) Representative immunofluorescent images of dorsal skin from mice treated as in A. Staining with anti-keratin14 (KRT14; green) marking epidermal layer and Ki67 (purple) marking the HF bulb. DAPI stain in blue. Scale bar 100μm. (E) Quantification of normalized Ki67 MFI signal in the peri-follicular area of dorsal skin from mice treated as in A. Data combined from 4 regions of interest (ROI) per mouse taken from 5 TRPV1 activated mice and 9 controls (****p<0.0001). (F) Diagram of experimental design and representative images from TRPV1 activated mice and controls treated with CNO on half of their back skin (marked with dashed rectangle). Anti-Spp1 neutralizing antibody or IgG control were injected intradermally to the same skin area. Data are combined from 4 HFs per mouse collected from 6 controls, 3 TRPV1 activated + IgG treated and 4 TRPV1 activated + anti-Spp1 treated mice (****p<0.0001). (G-H) Percentage of CD9+CD26+ dermal fibroblasts from TRPV1 activated mice and their controls intradermally injected with (G) QWF (SubP antagonist) or vehicle (**p=0.005, ***p=0.0004), (H) CGRP8–37 (CGRP antagonist) or vehicle (***p=0.0001, ****p<0.0001). (I) Diagram of experimental design and representative images from TRPV1 activated mice and controls pre-treated intradermally with CGRP8–37 or vehicle and monitored for hair coat growth for 14 days. Quantification of HF length from 6 to 8 HFs per mouse, taken from 3–6 mice per group (****p<0.0001). (J) Representative immunofluorescent images of dorsal skin from mice treated as in I. Stained with anti-KRT14 (green), Ki67 (pink), and DAPI (blue). Scale bar, 100μm.

Article Snippet: CGRP 8-37 (rat) , Tocris , Cat# 1169.

Techniques: Activation Assay, Staining, Control, Injection

(A) Quantification of TUNEL+ F4/80+ cell number per field of view from dorsal skin of TRPV1 activated mice and controls 3.5 hours after a single intradermal CNO treatment. Data are combined from 6 to 7 fields of view per mouse, taken from 7 mice per group (****p<0.0001). (B) Representative immunofluorescent images of 20μm skin sections from mice treated as in A. Sections stained with anti-F4/80 (red), TUNEL (green) and DAPI (blue). White arrowheads indicate F4/80+ TUNEL+ cells. Scale bar 50μm. (C) Percentage of Annexin V+ dermal macrophages from dorsal skin of TRPV1 activated mice and controls 45 minutes after a single CNO intradermal injection (***p=0.0002). (D) Mice back skin intradermally injected with CGRP on one side and vehicle on the other. (Left) Samples collected 45 minutes later and stained for annexin V as in C (*p-paired=0.017). (Right) samples collected 6 hours later and dermal macrophage frequency assessed (*p-paired=0.015). (E) Representative immunofluorescent images of 150μm dorsal skin sections from TRPV1 activated mice and controls pretreated with CGRP8–37 or vehicle followed by single intradermal CNO injection. Samples collected 6 hours later and stained with anti-F4/80 (red), CD207 (green), and DAPI (blue). Dashed rectangles indicate the lower follicle and peri-follicular area. Scale bar 100μm. (F) Quantification of F4/80 normalized MFI signal in the peri-follicular area from mice treated as in E. Data are combined from 6–8 ROIs per mouse taken from 5–8 mice per group (****p<0.0001). (G) Percentage of dermal macrophages from TRPV1 activated mice and controls treated as in E (*p=0.048,0.012,****p<0.0001). (H) Dermal macrophages frequency in dorsal skin of TRPV1 activated mice and controls reconstituted with Ramp1 KO or wild type BM. Chimeric mice given a single CNO injection and data collected 6 hours later (*p=0.04,***p=0.0009). (I) Dermal macrophages frequency in dorsal skin of TRPV1 activated mice and controls reconstituted with CD64Cre Ramp1+/+ or CD64Cre Ramp1fl/fl BM. Mice treated with CNO as in H (*p=0.043,***p=0.0001).

Journal: Developmental cell

Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice

doi: 10.1016/j.devcel.2024.05.019

Figure Lengend Snippet: (A) Quantification of TUNEL+ F4/80+ cell number per field of view from dorsal skin of TRPV1 activated mice and controls 3.5 hours after a single intradermal CNO treatment. Data are combined from 6 to 7 fields of view per mouse, taken from 7 mice per group (****p<0.0001). (B) Representative immunofluorescent images of 20μm skin sections from mice treated as in A. Sections stained with anti-F4/80 (red), TUNEL (green) and DAPI (blue). White arrowheads indicate F4/80+ TUNEL+ cells. Scale bar 50μm. (C) Percentage of Annexin V+ dermal macrophages from dorsal skin of TRPV1 activated mice and controls 45 minutes after a single CNO intradermal injection (***p=0.0002). (D) Mice back skin intradermally injected with CGRP on one side and vehicle on the other. (Left) Samples collected 45 minutes later and stained for annexin V as in C (*p-paired=0.017). (Right) samples collected 6 hours later and dermal macrophage frequency assessed (*p-paired=0.015). (E) Representative immunofluorescent images of 150μm dorsal skin sections from TRPV1 activated mice and controls pretreated with CGRP8–37 or vehicle followed by single intradermal CNO injection. Samples collected 6 hours later and stained with anti-F4/80 (red), CD207 (green), and DAPI (blue). Dashed rectangles indicate the lower follicle and peri-follicular area. Scale bar 100μm. (F) Quantification of F4/80 normalized MFI signal in the peri-follicular area from mice treated as in E. Data are combined from 6–8 ROIs per mouse taken from 5–8 mice per group (****p<0.0001). (G) Percentage of dermal macrophages from TRPV1 activated mice and controls treated as in E (*p=0.048,0.012,****p<0.0001). (H) Dermal macrophages frequency in dorsal skin of TRPV1 activated mice and controls reconstituted with Ramp1 KO or wild type BM. Chimeric mice given a single CNO injection and data collected 6 hours later (*p=0.04,***p=0.0009). (I) Dermal macrophages frequency in dorsal skin of TRPV1 activated mice and controls reconstituted with CD64Cre Ramp1+/+ or CD64Cre Ramp1fl/fl BM. Mice treated with CNO as in H (*p=0.043,***p=0.0001).

Article Snippet: CGRP 8-37 (rat) , Tocris , Cat# 1169.

Techniques: TUNEL Assay, Staining, Injection

Journal: Developmental cell

Article Title: Dermal TRPV1 innervations engage a macrophage and fibroblast containing pathway to activate hair growth in mice

doi: 10.1016/j.devcel.2024.05.019

Figure Lengend Snippet: Key resources table

Article Snippet: CGRP 8-37 (rat) , Tocris , Cat# 1169.

Techniques: Recombinant, RNAscope, Multiplex Assay, In Situ, Software

Fig. 1 Chronic NTG injection evoked sustained CM-like phenotypes. A Schematic illustration of chronic NTG injection protocol. Mice of both sexes were i.p. injected with either vehicle (Ctrl) or NTG (0.1 mg/kg). B On day 1, the basal mechanical threshold was the same between the NTG and control group, while the formal developed mechanical hyperalgesia after 2 hrs post-treatment (left, n = 18 per group; p < 0.01 **, and p < 0.001 ***). Sustained basal mechanical hyperalgesia developed after repeated doses of NTG administration (right, n = 18 per group; p < 0.001 ***). C The basal mechanical threshold recovered 6 days after the final NTG injection (n = 4 per group; F(1,24) = 16.2; p < 0.05 *, and p < 0.01 **). D Schematic illustration of periorbital test protocol. The periorbital responses were scored 2 hrs after the i.p. injection of the NTG (left). Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in both sexes of mice (right, n = 9 per group; F(1,112) = 117.8; p < 0.05 *, p < 0.01 **, and p < 0.001 ***). E Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in male mice (n = 5 per group; F(1,4) = 71.6; p < 0.05 *, and p < 0.001 ***). F Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in female mice (n = 4 per group; p < 0.05 *, and p < 0.01 **). G Schematic illustration of acute sumatriptan treatment protocol. Mice of both sexes were i.p. injected with sumatriptan (0.6 mg/kg) 5 min after NTG injection on day 9 (left). Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia on day 9. The basal response in the NTG group returned to mechanical hyperalgesia on day 10, suggesting that acute sumatriptan treatment only aborted acute pain but did not reverse the chronicity of mechanical hyperalgesia. (right, n = 20 per group; p < 0.001 ***). H Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia in male mice (n = 10 per group; p < 0.05 *, and p < 0.01 **). I Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia in female mice (n = 10 per group, p < 0.001 ***). J Schematic illustration of chronic NTG injection protocol. Mice were sacrificed after the NTG post-treatment von Frey test on day 9. K Representative images show that co-labeled CGRP and pERK neurons in the TG after chronic NTG administration were significantly higher than that in the controls (right, n = 4 per group; p = 0.043). Scale bar: 200 μm. l Quantification of the coloalized percentage of CGRP and pERK-positive neurons in the TG after chronic NTG induction (n = 4 per group; p = 0.003). All data shown are mean ± SEM and analyzed by Friedman tests with Dunn’s post hoc test (B, F, G-I) or Bonferroni post hoc test (C-E) or Mann-Whitney U test (K, L). Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Journal: The journal of headache and pain

Article Title: CGRP-dependent sensitization of PKC-δ positive neurons in central amygdala mediates chronic migraine.

doi: 10.1186/s10194-022-01531-8

Figure Lengend Snippet: Fig. 1 Chronic NTG injection evoked sustained CM-like phenotypes. A Schematic illustration of chronic NTG injection protocol. Mice of both sexes were i.p. injected with either vehicle (Ctrl) or NTG (0.1 mg/kg). B On day 1, the basal mechanical threshold was the same between the NTG and control group, while the formal developed mechanical hyperalgesia after 2 hrs post-treatment (left, n = 18 per group; p < 0.01 **, and p < 0.001 ***). Sustained basal mechanical hyperalgesia developed after repeated doses of NTG administration (right, n = 18 per group; p < 0.001 ***). C The basal mechanical threshold recovered 6 days after the final NTG injection (n = 4 per group; F(1,24) = 16.2; p < 0.05 *, and p < 0.01 **). D Schematic illustration of periorbital test protocol. The periorbital responses were scored 2 hrs after the i.p. injection of the NTG (left). Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in both sexes of mice (right, n = 9 per group; F(1,112) = 117.8; p < 0.05 *, p < 0.01 **, and p < 0.001 ***). E Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in male mice (n = 5 per group; F(1,4) = 71.6; p < 0.05 *, and p < 0.001 ***). F Sustained mechanical hyperalgesia developed after repeated doses of NTG administration in female mice (n = 4 per group; p < 0.05 *, and p < 0.01 **). G Schematic illustration of acute sumatriptan treatment protocol. Mice of both sexes were i.p. injected with sumatriptan (0.6 mg/kg) 5 min after NTG injection on day 9 (left). Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia on day 9. The basal response in the NTG group returned to mechanical hyperalgesia on day 10, suggesting that acute sumatriptan treatment only aborted acute pain but did not reverse the chronicity of mechanical hyperalgesia. (right, n = 20 per group; p < 0.001 ***). H Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia in male mice (n = 10 per group; p < 0.05 *, and p < 0.01 **). I Acute sumatriptan injection transiently alleviated chronic NTG induced mechanical hyperalgesia in female mice (n = 10 per group, p < 0.001 ***). J Schematic illustration of chronic NTG injection protocol. Mice were sacrificed after the NTG post-treatment von Frey test on day 9. K Representative images show that co-labeled CGRP and pERK neurons in the TG after chronic NTG administration were significantly higher than that in the controls (right, n = 4 per group; p = 0.043). Scale bar: 200 μm. l Quantification of the coloalized percentage of CGRP and pERK-positive neurons in the TG after chronic NTG induction (n = 4 per group; p = 0.003). All data shown are mean ± SEM and analyzed by Friedman tests with Dunn’s post hoc test (B, F, G-I) or Bonferroni post hoc test (C-E) or Mann-Whitney U test (K, L). Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Article Snippet: Stereotactic or cannula microinfusion of calcitonin gene‐related peptide receptor antagonist into CeA To block the PBN CGRP neurotransmission to the CeA, we applied the CGRP receptor 1 antagonist, CGRP fragment 8–37 (HY-P0209, MedChemExpress), dissolved in normal saline at 1.8 μg/μl [19], into bilateral CeA with either acute stereotactic microinfusion or intermittent infusion via chronically implanted cannulas.

Techniques: Injection, Control, Labeling, MANN-WHITNEY

Fig. 3 Expression of CGRP after chronic NTG administration. A Schematic illustration of the rostro-caudal anatomical location of CeA relative to the position of bregma. B Representative images of CGRP expression in the CeA after chronic NTG administration. Red dashed square indicates the high magnification of the CeA (left). The CGRP fiber intensity in the CeA after chronic NTG induction was significantly higher than that in the control group (right, n = 4 per group; CeA_R; p = 0.003; CeA_L; p = 0.0003). Scale bar: 1 mm (left), 50 μm (right). C The representative pERK positive neurons double-labeled with CGRP fibers. Scale bar: 100 μm. D Representative low and high magnification images of co-labeled CGRP receptor type 1 (CGRPR)- and PKC-δ- positive neurons in the CeA (left) and quantified results (right, n = 4 per group; CGRPR/PKC-δ; p = 0.593; PKC-δ/CGRPR; p = 0.687). Scale bar: 50 μm. E Representative low magnification images of co-labeled CGRP- and pERK- positive neurons in the PBN. Scale bar: 500 μm. F Representative low and high magnification images of co-labeled CGRP- and pERK- positive neurons in the PBN (left). The CGRP positive neurons in the PBN was significantly higher after chronic NTG administration than controls (right, n = 4 per group; CGRP/pERK; p < 0.0001; pERK/ CGRP; p = 0.002). Scale bar: 100 μm. G Representative images of bilateral retrograde CTB594 labeling and co-labeled CGRP fibers in the CeA. Scale bar: 100 μm. H Representative images of CTB594 co-labeled CGRP positive neurons in the PBN, confirming that the CGRP positive neurons project from the PBN to CeA (left). The CGRP positive neurons in the PBN was significantly higher after chronic NTG administration than controls (right, n = 4 per group; CTB594/CGRP; p = 0.002; CGRP/CTB594; p = 0.0006). Scale bar: 100 μm. All data shown are mean ± SEM and analyzed by Mann-Whitney U test. Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Journal: The journal of headache and pain

Article Title: CGRP-dependent sensitization of PKC-δ positive neurons in central amygdala mediates chronic migraine.

doi: 10.1186/s10194-022-01531-8

Figure Lengend Snippet: Fig. 3 Expression of CGRP after chronic NTG administration. A Schematic illustration of the rostro-caudal anatomical location of CeA relative to the position of bregma. B Representative images of CGRP expression in the CeA after chronic NTG administration. Red dashed square indicates the high magnification of the CeA (left). The CGRP fiber intensity in the CeA after chronic NTG induction was significantly higher than that in the control group (right, n = 4 per group; CeA_R; p = 0.003; CeA_L; p = 0.0003). Scale bar: 1 mm (left), 50 μm (right). C The representative pERK positive neurons double-labeled with CGRP fibers. Scale bar: 100 μm. D Representative low and high magnification images of co-labeled CGRP receptor type 1 (CGRPR)- and PKC-δ- positive neurons in the CeA (left) and quantified results (right, n = 4 per group; CGRPR/PKC-δ; p = 0.593; PKC-δ/CGRPR; p = 0.687). Scale bar: 50 μm. E Representative low magnification images of co-labeled CGRP- and pERK- positive neurons in the PBN. Scale bar: 500 μm. F Representative low and high magnification images of co-labeled CGRP- and pERK- positive neurons in the PBN (left). The CGRP positive neurons in the PBN was significantly higher after chronic NTG administration than controls (right, n = 4 per group; CGRP/pERK; p < 0.0001; pERK/ CGRP; p = 0.002). Scale bar: 100 μm. G Representative images of bilateral retrograde CTB594 labeling and co-labeled CGRP fibers in the CeA. Scale bar: 100 μm. H Representative images of CTB594 co-labeled CGRP positive neurons in the PBN, confirming that the CGRP positive neurons project from the PBN to CeA (left). The CGRP positive neurons in the PBN was significantly higher after chronic NTG administration than controls (right, n = 4 per group; CTB594/CGRP; p = 0.002; CGRP/CTB594; p = 0.0006). Scale bar: 100 μm. All data shown are mean ± SEM and analyzed by Mann-Whitney U test. Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Techniques: Expressing, Control, Labeling, MANN-WHITNEY

Fig. 5 Chemogenetic inhibition of the PKC-δ positive neurons in the CeA. A Schematic illustration of bilateral AAV5-DIO-mCherry (mCherry) or AAV5-DIO-hM4Di-mCherry (hM4Di) injection in the CeA of PKC-δ-Cre mouse. B Schematic illustration of experimental timeline. After 3 weeks of virus expression, PKC-δ-Cre mice were i.p. injected with either vehicle (Ctrl) or NTG (0.1 mg/kg) every other day to day 9 (totally 5 injections) and i.p. injected with CNO (5 mg/kg) on day 10 and 12. The mechanical threshold tested 2 hrs post-treatment after the NTG injection and 1 hr. post-treatment after the CNO injection. C Representative low (up) and high magnification (down) images of mCherry injection sites, confirming the correct injection of viral vectors or controls at bilateral CeA. Scale bar: 100 μm. D Behavioral consequences before and after CNO application PKC-δ-Cre mice pretreated with bilateral hM4Di virus injection in the CeA after chronic vehicle or NTG administration. Sustained mechanical hyperalgesia alleviated 1 hr. after the CNO application on day 10 and 12 (left, n = 4 per group; p < 0.05 *, and p < 0.01 **) while the marble burying test was unaffected (right, n = 4 per group) (E) Sustained basal mechanical hyperalgesia developed after repeated doses of NTG administration in both mCherry and hM4Di group (n = 6 per group). F Behavioral consequences before and after CNO application PKC-δ-Cre mice pretreated with bilateral mCherry and hM4Di virus injection in the CeA and chronic NTG administration. Sustained mechanical hyperalgesia alleviated 1 hr. after the CNO application on day 10 and 12 (left, n = 6 per group; p < 0.01 **, and p < 0.001 ***) while the marble burying test was unaffected (right, n = 6 per group). (G) Representative images of pERK positive neurons in the TG with or without CNO application (left). The numbers of pERK positive neurons in the TG were significantly decreased after the CNO application (right, n = 4 per group; p = 0.009). Scale bar: 100 μm. H The percentage of CGRP/ pERK positive neurons in the TG were significantly decreased after the CNO application (n = 4 per group; p = 0.005). All data shown are mean ± SEM and analyzed by Friedman tests with Dunn’s post hoc test (D, F) or Mann-Whitney U test (G, H). Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Journal: The journal of headache and pain

Article Title: CGRP-dependent sensitization of PKC-δ positive neurons in central amygdala mediates chronic migraine.

doi: 10.1186/s10194-022-01531-8

Figure Lengend Snippet: Fig. 5 Chemogenetic inhibition of the PKC-δ positive neurons in the CeA. A Schematic illustration of bilateral AAV5-DIO-mCherry (mCherry) or AAV5-DIO-hM4Di-mCherry (hM4Di) injection in the CeA of PKC-δ-Cre mouse. B Schematic illustration of experimental timeline. After 3 weeks of virus expression, PKC-δ-Cre mice were i.p. injected with either vehicle (Ctrl) or NTG (0.1 mg/kg) every other day to day 9 (totally 5 injections) and i.p. injected with CNO (5 mg/kg) on day 10 and 12. The mechanical threshold tested 2 hrs post-treatment after the NTG injection and 1 hr. post-treatment after the CNO injection. C Representative low (up) and high magnification (down) images of mCherry injection sites, confirming the correct injection of viral vectors or controls at bilateral CeA. Scale bar: 100 μm. D Behavioral consequences before and after CNO application PKC-δ-Cre mice pretreated with bilateral hM4Di virus injection in the CeA after chronic vehicle or NTG administration. Sustained mechanical hyperalgesia alleviated 1 hr. after the CNO application on day 10 and 12 (left, n = 4 per group; p < 0.05 *, and p < 0.01 **) while the marble burying test was unaffected (right, n = 4 per group) (E) Sustained basal mechanical hyperalgesia developed after repeated doses of NTG administration in both mCherry and hM4Di group (n = 6 per group). F Behavioral consequences before and after CNO application PKC-δ-Cre mice pretreated with bilateral mCherry and hM4Di virus injection in the CeA and chronic NTG administration. Sustained mechanical hyperalgesia alleviated 1 hr. after the CNO application on day 10 and 12 (left, n = 6 per group; p < 0.01 **, and p < 0.001 ***) while the marble burying test was unaffected (right, n = 6 per group). (G) Representative images of pERK positive neurons in the TG with or without CNO application (left). The numbers of pERK positive neurons in the TG were significantly decreased after the CNO application (right, n = 4 per group; p = 0.009). Scale bar: 100 μm. H The percentage of CGRP/ pERK positive neurons in the TG were significantly decreased after the CNO application (n = 4 per group; p = 0.005). All data shown are mean ± SEM and analyzed by Friedman tests with Dunn’s post hoc test (D, F) or Mann-Whitney U test (G, H). Significance levels set at p < 0.05 *, p < 0.01 **, and p < 0.001 ***

Techniques: Inhibition, Injection, Virus, Expressing, MANN-WHITNEY

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