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cyclosomatostatin  (Tocris)


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    Structured Review

    Tocris cyclosomatostatin
    Cyclosomatostatin, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cyclosomatostatin/Cyclosomatostatin/pm41895668-54-20-24
    Average 93 stars, based on 15 article reviews
    cyclosomatostatin - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Centrifugation:

    Article Title: Somatostatin and insulin mediate glucose-inhibited glucagon secretion in the pancreatic α-cell by lowering cAMP
    Article Snippet: .. Twelve to fifteen islets were transferred to buffer with 1 or 11 mM glucose with and without the following drugs (from Sigma, unless otherwise specified): 300 μM 8-bromoadenosine 3′,5′-cyclic monophosphate (8-Br-cAMP), 300 μM 8-(4-chlorophenylthio)-2′- O -methyladenosine 3′,5′-cyclic monophosphate monosodium hydrate (8- O -Me-CPT), 300 μM N6-benzoyladenosine-3′,5′-cyclic monophosphate sodium salt (6-Bnz-cAMP), 100 nM or 1 μM insulin, 100 nM somatostatin, 1 μM S961 (Novo Nordisk, Princeton, NJ), 50 μM forskolin, 100 μM 3-isobutyl-1-methylxanthine (IBMX), 100 μM Rp-cAMPS, 250 nM cyclosomatostatin (Tocris Bioscience, Minneapolis, MN), and/or 200 nM CYN154806 (Tocris Bioscience) for 45 min at 37°C before centrifugation and supernatant collection. ..

    other:

    Article Title: Somatostatin released by single O-LM interneurons slowly inhibits intrinsic neuronal excitability in a paracrine and autocrine manner
    Article Snippet: BAPTA, SST-14, Cyclosomatostatin, CYN154806, Octreotide, NBQX, Carbachol (Carbamoylcholine chloride) were obtained from Tocris.

    Sonication:

    Article Title: Somatostatin-induced modulation of microglial activity contributes to mitigating Alzheimer's disease pathology.
    Article Snippet: Somatostatin (SST) is a neuropeptide widely expressed in the central nervous system, known to exert inhibitory effects through the activation of G protein-coupled somatostatin receptors (SSTRs).. Although its synaptic and network-level functions have been implicated in various neurological disorders, the direct peptidergic actions of SST—particularly on microglia—remain poorly understood.. Given that SST levels are reduced in Alzheimer’s disease (AD) and that microglia predominantly express SSTR2, we hypothesized that SST modulates microglial function in both physiological and AD-related contexts.

    Concentration Assay:

    Article Title: Somatostatin signaling via SSTR1 contributes to the quiescence of colon cancer stem cells
    Article Snippet: .. HT29 and SW480 cells were treated with 10 uM cyclosomatostatin (Tocris), which is within the accepted concentration range used to inhibit SST signaling without affecting cell viability [ ]. ..

    Incubation:

    Article Title: Royal jelly coordinately enhances hippocampal neuronal expression of somatostatin and neprilysin genes conferring neuronal protection against toxic soluble amyloid-β oligomers implicated in Alzheimer’s disease pathogenesis
    Article Snippet: Hippocampal somatostatin (SST)-neprilysin (NEP) system functions as a defense system against neurotoxic soluble amyloid-β oligomers associated with onset of Alzheimer’s disease.. However, it remains unknown whether royal jelly (RJ) could impact the defense system.. In this study using primary cultures of hippocampal neurons, including SST-positive and NEP-positive neuronal subsets, we evaluated the ability of DMSO-soluble fraction of RJ (DRJ) to enhance SST and NEP genes expression.

    Synthesized:

    Article Title: Royal jelly coordinately enhances hippocampal neuronal expression of somatostatin and neprilysin genes conferring neuronal protection against toxic soluble amyloid-β oligomers implicated in Alzheimer’s disease pathogenesis
    Article Snippet: Hippocampal somatostatin (SST)-neprilysin (NEP) system functions as a defense system against neurotoxic soluble amyloid-β oligomers associated with onset of Alzheimer’s disease.. However, it remains unknown whether royal jelly (RJ) could impact the defense system.. In this study using primary cultures of hippocampal neurons, including SST-positive and NEP-positive neuronal subsets, we evaluated the ability of DMSO-soluble fraction of RJ (DRJ) to enhance SST and NEP genes expression.

    In Vitro:

    Article Title: Royal jelly coordinately enhances hippocampal neuronal expression of somatostatin and neprilysin genes conferring neuronal protection against toxic soluble amyloid-β oligomers implicated in Alzheimer’s disease pathogenesis
    Article Snippet: Hippocampal somatostatin (SST)-neprilysin (NEP) system functions as a defense system against neurotoxic soluble amyloid-β oligomers associated with onset of Alzheimer’s disease.. However, it remains unknown whether royal jelly (RJ) could impact the defense system.. In this study using primary cultures of hippocampal neurons, including SST-positive and NEP-positive neuronal subsets, we evaluated the ability of DMSO-soluble fraction of RJ (DRJ) to enhance SST and NEP genes expression.

    Recombinant:

    Article Title: Royal jelly coordinately enhances hippocampal neuronal expression of somatostatin and neprilysin genes conferring neuronal protection against toxic soluble amyloid-β oligomers implicated in Alzheimer’s disease pathogenesis
    Article Snippet: Hippocampal somatostatin (SST)-neprilysin (NEP) system functions as a defense system against neurotoxic soluble amyloid-β oligomers associated with onset of Alzheimer’s disease.. However, it remains unknown whether royal jelly (RJ) could impact the defense system.. In this study using primary cultures of hippocampal neurons, including SST-positive and NEP-positive neuronal subsets, we evaluated the ability of DMSO-soluble fraction of RJ (DRJ) to enhance SST and NEP genes expression.



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    (A) Diffusion area in dLS of a fluorescent tracer injected through a cannula. (B) Injection of the SSTR pan-antagonist <t>cyclosomatostatin</t> (2 μg/side (62,63)) in LS improved social-fear extinction deficits of Magel2KO mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SSTR antagonism F(4,55)=2.7 p=0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi2 p=0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM). Mann Whitney test comparing antagonist and vehicle groups p=0.3. (E) Injection of the SSTR agonist SST14 (1 ng/side, (64,65)) in LS impaired social-fear extinction of Magel2WT mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SST F(4,50)=4 p=0.006 post-hoc Sidak test. (F) Discrimination between stimulus mice decreased with SST14 compared to NaCl-injected WT-controls (Chi2 p=0.002). (G) Cumulated time of attacks on the 6 stimulus mice not affected by SST14 in LS (means±SEM). Mann Whitney test comparing SST14 and NaCl groups p=0.06 (non-significant trend).
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    (A) Diffusion area in dLS of a fluorescent tracer injected through a cannula. (B) Injection of the SSTR pan-antagonist <t>cyclosomatostatin</t> (2 μg/side (62,63)) in LS improved social-fear extinction deficits of Magel2KO mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SSTR antagonism F(4,55)=2.7 p=0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi2 p=0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM). Mann Whitney test comparing antagonist and vehicle groups p=0.3. (E) Injection of the SSTR agonist SST14 (1 ng/side, (64,65)) in LS impaired social-fear extinction of Magel2WT mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SST F(4,50)=4 p=0.006 post-hoc Sidak test. (F) Discrimination between stimulus mice decreased with SST14 compared to NaCl-injected WT-controls (Chi2 p=0.002). (G) Cumulated time of attacks on the 6 stimulus mice not affected by SST14 in LS (means±SEM). Mann Whitney test comparing SST14 and NaCl groups p=0.06 (non-significant trend).
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    Figure 4: Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of <t>SG-cSst</t> mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. *,**p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.
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    Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of <t>SG-cSst</t> mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment × surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. ∗,∗∗p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.
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    Tocris recombinant proteins picrotoxin hello bio hb0506 cgp 55845 tocris 1248 sst 14 bachem h 1490 cyclosomatostatin cyclo sst
    Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of <t>SG-cSst</t> mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment × surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. ∗,∗∗p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.
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    Image Search Results


    (A) Diffusion area in dLS of a fluorescent tracer injected through a cannula. (B) Injection of the SSTR pan-antagonist cyclosomatostatin (2 μg/side (62,63)) in LS improved social-fear extinction deficits of Magel2KO mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SSTR antagonism F(4,55)=2.7 p=0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi2 p=0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM). Mann Whitney test comparing antagonist and vehicle groups p=0.3. (E) Injection of the SSTR agonist SST14 (1 ng/side, (64,65)) in LS impaired social-fear extinction of Magel2WT mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SST F(4,50)=4 p=0.006 post-hoc Sidak test. (F) Discrimination between stimulus mice decreased with SST14 compared to NaCl-injected WT-controls (Chi2 p=0.002). (G) Cumulated time of attacks on the 6 stimulus mice not affected by SST14 in LS (means±SEM). Mann Whitney test comparing SST14 and NaCl groups p=0.06 (non-significant trend).

    Journal: Biological psychiatry

    Article Title: Disengagement of somatostatin neurons from lateral septum circuitry by oxytocin and vasopressin restores social-fear extinction and suppresses aggression outbursts in Prader-Willi syndrome model

    doi: 10.1016/j.biopsych.2023.10.016

    Figure Lengend Snippet: (A) Diffusion area in dLS of a fluorescent tracer injected through a cannula. (B) Injection of the SSTR pan-antagonist cyclosomatostatin (2 μg/side (62,63)) in LS improved social-fear extinction deficits of Magel2KO mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SSTR antagonism F(4,55)=2.7 p=0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi2 p=0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM). Mann Whitney test comparing antagonist and vehicle groups p=0.3. (E) Injection of the SSTR agonist SST14 (1 ng/side, (64,65)) in LS impaired social-fear extinction of Magel2WT mice. Arrows indicate the onset of injection. Bold lines are means±SEM, light line individual subjects (N). Two-way ANOVA: time × SST F(4,50)=4 p=0.006 post-hoc Sidak test. (F) Discrimination between stimulus mice decreased with SST14 compared to NaCl-injected WT-controls (Chi2 p=0.002). (G) Cumulated time of attacks on the 6 stimulus mice not affected by SST14 in LS (means±SEM). Mann Whitney test comparing SST14 and NaCl groups p=0.06 (non-significant trend).

    Article Snippet: Two-way ANOVA: time × SSTR antagonism F (4,55) =2.7 p =0.03 post-hoc Sidak test. (C) Discrimination between stimulus mice during extinction increased with cyclosomatostatin compared to NaCl-injected KO-controls (Chi 2 p =0.001). (D) Cumulated time of attacks on the 6 stimulus mice not affected by cyclosomatostatin in LS (means±SEM).

    Techniques: Diffusion-based Assay, Injection, MANN-WHITNEY

    Figure 4: Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of SG-cSst mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. *,**p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.

    Journal: Molecular metabolism

    Article Title: Inhibition of somatostatin enhances the long-term metabolic outcomes of sleeve gastrectomy in mice.

    doi: 10.1016/j.molmet.2024.101979

    Figure Lengend Snippet: Figure 4: Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of SG-cSst mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n ¼ 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. *,**p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.

    Article Snippet: Cyclosomatostatin treatment Cyclosomatostatin (cSst) was purchased from Tocris (Cat. No. 3493) and dissolved to a final concentration of 0.08% EtOH and saline. cSst was injected subcutaneously at 30 mg/kg body weight every evening from 7 days after the surgery until the end of the experiment.

    Techniques: Inhibition, Saline, Clinical Proteomics, Staining

    Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of SG-cSst mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment × surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. ∗,∗∗p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.

    Journal: Molecular Metabolism

    Article Title: Inhibition of somatostatin enhances the long-term metabolic outcomes of sleeve gastrectomy in mice

    doi: 10.1016/j.molmet.2024.101979

    Figure Lengend Snippet: Long-term response of obese mice to SG followed by inhibition of somatostatin signaling. A. Change in weight of SG-cSst mice (purple triangles) and SG-saline mice (black triangles), sham-cSst mice (green circles) and sham-saline mice (black squares). p < 0.01 by treatment and by treatment × surgery interaction by 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. B. Glucose levels following an oral mixed meal tolerance test. Colors as in A. p < 0.01 by treatment 3-way repeated measurement ANOVA. Error bars denote SEM. n = 7,7,9,9. C. Area under the curve (AUC) for the mixed meals tolerance test. D. Fasting plasma insulin levels at the end of the experiment. E,F. Fasting (E) and post-prandial (F) plasma GLP-1 levels at the end of the experiment. G. Post-prandial total cholesterol, HDL-cholesterol, and LDL-cholesterol in the plasma at the end of the experiment. H. Quantification of hepatic steatosis by percent of the area covered by lipid droplets in a hematoxylin and eosin staining. ∗,∗∗p < 0.05, p < 0.01 by Tukey post-hoc test (A,F,G,H). ##p < 0.01 by surgery in 2-way ANOVA.

    Article Snippet: Cyclosomatostatin (cSst) was purchased from Tocris (Cat. No. 3493) and dissolved to a final concentration of 0.08% EtOH and saline. cSst was injected subcutaneously at 30 μg/kg body weight every evening from 7 days after the surgery until the end of the experiment.

    Techniques: Inhibition, Saline, Clinical Proteomics, Staining