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  • 93
    Tocris cp 94253
    (a) Treatment with <t>CP-94253</t> (1–100 nM) for ten minutes increased phosphorylation of ERK1 and ERK2 in N2A-1B cells compared to unstimulated N2A-1B control cells treated with vehicle (PBS), but this was blocked by pretreatment with the antagonist SB-224289 (pERK1 F1,24 = 34.07, p < 0.0001; pERK2 F1,24 = 28.38, p < 0.0001). (b) No change was observed in total ERK in N2A-1B cells (total ERK1 F1,18 = 0.89, p = 0.36; total ERK2 F1,18 = 1.79, p = 0.20). (c) No change was observed in phospho-ERK1/2 with agonist treatment in untransfected wild-type N2A cells (pERK1 F1,24 = 3.62, p = 0.07; pERK2 F1,24 = 3.52, p = 0.07). Agonist treatment did not change levels of (d) phospho-p38 (F1,18 = 0.58, p = 0.46), (e) phospho-p54 JNK (F1,18 = 0.06, p = 0.81), and (f) phospho-p46 JNK (F1,18 = 0.21, p = 0.65). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 4–5 independent biological replicates (two-way ANOVA; ****p < 0.00001).
    Cp 94253, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 93 stars, based on 1 article reviews
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    86
    Pfizer Inc cp 94253
    Effects of RU 24969 (left) and <t>CP</t> <t>94253</t> (right) at various doses on PS in 5-HT1B+/+ (open symbols) and 5-HT1B−/− (filled symbols) mice during the 4 hr after injection in which an effect was observed. Results are expressed as minutes (mean ± SEM of 8 mice in each group for RU 24969 and 6 mice for CP 94253; 5–8 tests for each dose). *p < 0.05, significantly different from baseline (0 on abscissa); paired Student’st test. Complete set of data is available on request.
    Cp 94253, supplied by Pfizer Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cp 94253/product/Pfizer Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cp 94253 - by Bioz Stars, 2024-04
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    86
    Bio-Techne corporation cp 94253
    Cylinder test is a well-established spontaneous motor test based on limb-use asymmetry known to be sensitive to graft-induced functional recovery (A). All animals were severely impaired in the use of left forelimb (contralateral to the lesion side, open bars in A). 5HT grafts were functionally ineffective, whereas DA grafts ameliorated the limb use deficit significantly at 12 weeks after grafting (Two-way ANOVA F (5,163) = 16.75, p<0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0083). The animals were then challenged with L-DOPA to assess if the grafts were able to modulate the dyskinesia that were established prior to transplantation (B; two-way ANOVA F (8,245) = 63.48, p = <0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0033). DA-cell rich grafts reduced the dyskinesia, while 5HT cells were ineffective or even aggravated the dyskinesia. Co-treatment of the animals with 5HT receptor 1A and 1B agonists (0.1 mg/kg 8-OH-DPAT and 1.75 mg/kg <t>CP-94253)</t> reduced the dyskinesia significantly in all groups (B). The residual abnormal movements were primarily due to differential duration of action of L-DOPA and the agonists (C). tx: transplantation, *: different from pre-tx baseline; +: different from post-tx 12 wks; #: different from 6OHDA lesion and 5HT groups.
    Cp 94253, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cp 94253/product/Bio-Techne corporation
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cp 94253 - by Bioz Stars, 2024-04
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    86
    Millipore cp 94253 hydrochloride
    Cylinder test is a well-established spontaneous motor test based on limb-use asymmetry known to be sensitive to graft-induced functional recovery (A). All animals were severely impaired in the use of left forelimb (contralateral to the lesion side, open bars in A). 5HT grafts were functionally ineffective, whereas DA grafts ameliorated the limb use deficit significantly at 12 weeks after grafting (Two-way ANOVA F (5,163) = 16.75, p<0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0083). The animals were then challenged with L-DOPA to assess if the grafts were able to modulate the dyskinesia that were established prior to transplantation (B; two-way ANOVA F (8,245) = 63.48, p = <0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0033). DA-cell rich grafts reduced the dyskinesia, while 5HT cells were ineffective or even aggravated the dyskinesia. Co-treatment of the animals with 5HT receptor 1A and 1B agonists (0.1 mg/kg 8-OH-DPAT and 1.75 mg/kg <t>CP-94253)</t> reduced the dyskinesia significantly in all groups (B). The residual abnormal movements were primarily due to differential duration of action of L-DOPA and the agonists (C). tx: transplantation, *: different from pre-tx baseline; +: different from post-tx 12 wks; #: different from 6OHDA lesion and 5HT groups.
    Cp 94253 Hydrochloride, supplied by Millipore, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cp 94253 hydrochloride/product/Millipore
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cp 94253 hydrochloride - by Bioz Stars, 2024-04
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      Buy from Supplier

    86
    Bio-Techne corporation cp 94253 hydrochloride
    Cylinder test is a well-established spontaneous motor test based on limb-use asymmetry known to be sensitive to graft-induced functional recovery (A). All animals were severely impaired in the use of left forelimb (contralateral to the lesion side, open bars in A). 5HT grafts were functionally ineffective, whereas DA grafts ameliorated the limb use deficit significantly at 12 weeks after grafting (Two-way ANOVA F (5,163) = 16.75, p<0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0083). The animals were then challenged with L-DOPA to assess if the grafts were able to modulate the dyskinesia that were established prior to transplantation (B; two-way ANOVA F (8,245) = 63.48, p = <0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0033). DA-cell rich grafts reduced the dyskinesia, while 5HT cells were ineffective or even aggravated the dyskinesia. Co-treatment of the animals with 5HT receptor 1A and 1B agonists (0.1 mg/kg 8-OH-DPAT and 1.75 mg/kg <t>CP-94253)</t> reduced the dyskinesia significantly in all groups (B). The residual abnormal movements were primarily due to differential duration of action of L-DOPA and the agonists (C). tx: transplantation, *: different from pre-tx baseline; +: different from post-tx 12 wks; #: different from 6OHDA lesion and 5HT groups.
    Cp 94253 Hydrochloride, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cp 94253 hydrochloride/product/Bio-Techne corporation
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    cp 94253 hydrochloride - by Bioz Stars, 2024-04
    86/100 stars
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    Image Search Results


    (a) Treatment with CP-94253 (1–100 nM) for ten minutes increased phosphorylation of ERK1 and ERK2 in N2A-1B cells compared to unstimulated N2A-1B control cells treated with vehicle (PBS), but this was blocked by pretreatment with the antagonist SB-224289 (pERK1 F1,24 = 34.07, p < 0.0001; pERK2 F1,24 = 28.38, p < 0.0001). (b) No change was observed in total ERK in N2A-1B cells (total ERK1 F1,18 = 0.89, p = 0.36; total ERK2 F1,18 = 1.79, p = 0.20). (c) No change was observed in phospho-ERK1/2 with agonist treatment in untransfected wild-type N2A cells (pERK1 F1,24 = 3.62, p = 0.07; pERK2 F1,24 = 3.52, p = 0.07). Agonist treatment did not change levels of (d) phospho-p38 (F1,18 = 0.58, p = 0.46), (e) phospho-p54 JNK (F1,18 = 0.06, p = 0.81), and (f) phospho-p46 JNK (F1,18 = 0.21, p = 0.65). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 4–5 independent biological replicates (two-way ANOVA; ****p < 0.00001).

    Journal: ACS chemical neuroscience

    Article Title: 5-HT 1B RECEPTOR-MEDIATED ACTIVATION OF ERK1/2 REQUIRES BOTH Gα i/o AND β-ARRESTIN PROTEINS

    doi: 10.1021/acschemneuro.8b00596

    Figure Lengend Snippet: (a) Treatment with CP-94253 (1–100 nM) for ten minutes increased phosphorylation of ERK1 and ERK2 in N2A-1B cells compared to unstimulated N2A-1B control cells treated with vehicle (PBS), but this was blocked by pretreatment with the antagonist SB-224289 (pERK1 F1,24 = 34.07, p < 0.0001; pERK2 F1,24 = 28.38, p < 0.0001). (b) No change was observed in total ERK in N2A-1B cells (total ERK1 F1,18 = 0.89, p = 0.36; total ERK2 F1,18 = 1.79, p = 0.20). (c) No change was observed in phospho-ERK1/2 with agonist treatment in untransfected wild-type N2A cells (pERK1 F1,24 = 3.62, p = 0.07; pERK2 F1,24 = 3.52, p = 0.07). Agonist treatment did not change levels of (d) phospho-p38 (F1,18 = 0.58, p = 0.46), (e) phospho-p54 JNK (F1,18 = 0.06, p = 0.81), and (f) phospho-p46 JNK (F1,18 = 0.21, p = 0.65). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 4–5 independent biological replicates (two-way ANOVA; ****p < 0.00001).

    Article Snippet: Treatment drugs used were: CP-94253, 56 SB-224289, 53 , gallein (Tocris), pertussis toxin (Novex), and U0126 (Cell Signaling).

    Techniques:

    CP-94253 (1–100 nM) produced dose-dependent increases in (a) ERK1 phosphorylation and (b) ERK2 phosphorylation in N2A cells expressing wild-type HA-5-HT1B receptors (WT-1B) compared to unstimulated N2A-1B control cells treated with vehicle (PBS). (a) At 100 nM of CP-94263, phospho-ERK1 levels were significantly decreased in cells expressing the S256A and S291A mutant receptors (S256A mutant p = 0.005; S291A mutant p = 0.033; S277A+S279A mutant p = 0.054; S154A mutant p = 0.104; T158A mutant p = 0.071; S154A+T158A mutant p = 0.184) compared to WT-1B cells. (b) Phospho-ERK2 levels were not significantly different between WT-1B and mutant cell lines with 100 nM of CP-94263 (S256A mutant p = 0.845; S291A mutant p = 0.996; S277A+S279A mutant p = 0.876; S154A mutant p = 0.999; T158A mutant p = 0.935; S154A+T158A mutant p > 0.999). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 3 independent biological replicates for each receptor (two-way ANOVA with Dunnett’s post-hoc tests; **p < 0.01, *p < 0.05).

    Journal: ACS chemical neuroscience

    Article Title: 5-HT 1B RECEPTOR-MEDIATED ACTIVATION OF ERK1/2 REQUIRES BOTH Gα i/o AND β-ARRESTIN PROTEINS

    doi: 10.1021/acschemneuro.8b00596

    Figure Lengend Snippet: CP-94253 (1–100 nM) produced dose-dependent increases in (a) ERK1 phosphorylation and (b) ERK2 phosphorylation in N2A cells expressing wild-type HA-5-HT1B receptors (WT-1B) compared to unstimulated N2A-1B control cells treated with vehicle (PBS). (a) At 100 nM of CP-94263, phospho-ERK1 levels were significantly decreased in cells expressing the S256A and S291A mutant receptors (S256A mutant p = 0.005; S291A mutant p = 0.033; S277A+S279A mutant p = 0.054; S154A mutant p = 0.104; T158A mutant p = 0.071; S154A+T158A mutant p = 0.184) compared to WT-1B cells. (b) Phospho-ERK2 levels were not significantly different between WT-1B and mutant cell lines with 100 nM of CP-94263 (S256A mutant p = 0.845; S291A mutant p = 0.996; S277A+S279A mutant p = 0.876; S154A mutant p = 0.999; T158A mutant p = 0.935; S154A+T158A mutant p > 0.999). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 3 independent biological replicates for each receptor (two-way ANOVA with Dunnett’s post-hoc tests; **p < 0.01, *p < 0.05).

    Article Snippet: Treatment drugs used were: CP-94253, 56 SB-224289, 53 , gallein (Tocris), pertussis toxin (Novex), and U0126 (Cell Signaling).

    Techniques: Produced, Expressing, Mutagenesis

    N2A-1B cells were pretreated for one hour with inhibitors prior to treatment with 100 nM CP-94253 for ten minutes and compared to unstimulated N2A-1B control cells treated with vehicle (PBS). (a) 5-HT1B-mediated phosphorylation of ERK1/2 was blocked by pertussis toxin (inhibitor effect: F2,18 = 7.98, p = 0.0033). (b) 5-HT1B-mediated phosphorylation of ERK1/2 was not sensitive gallein (inhibitor effect: F2,12 = 3.198, p = 0.077). (c) 5-HT1B-mediated phosphorylation of ERK1/2 was blocked by the MEK1/2 inhibitor U0126 (inhibitor effect: F2,12 = 13.34, p = 0.0009). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 3–4 independent biological replicates for each experiment (two-way ANOVA; ***p < 0.001, **p < 0.01).

    Journal: ACS chemical neuroscience

    Article Title: 5-HT 1B RECEPTOR-MEDIATED ACTIVATION OF ERK1/2 REQUIRES BOTH Gα i/o AND β-ARRESTIN PROTEINS

    doi: 10.1021/acschemneuro.8b00596

    Figure Lengend Snippet: N2A-1B cells were pretreated for one hour with inhibitors prior to treatment with 100 nM CP-94253 for ten minutes and compared to unstimulated N2A-1B control cells treated with vehicle (PBS). (a) 5-HT1B-mediated phosphorylation of ERK1/2 was blocked by pertussis toxin (inhibitor effect: F2,18 = 7.98, p = 0.0033). (b) 5-HT1B-mediated phosphorylation of ERK1/2 was not sensitive gallein (inhibitor effect: F2,12 = 3.198, p = 0.077). (c) 5-HT1B-mediated phosphorylation of ERK1/2 was blocked by the MEK1/2 inhibitor U0126 (inhibitor effect: F2,12 = 13.34, p = 0.0009). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 3–4 independent biological replicates for each experiment (two-way ANOVA; ***p < 0.001, **p < 0.01).

    Article Snippet: Treatment drugs used were: CP-94253, 56 SB-224289, 53 , gallein (Tocris), pertussis toxin (Novex), and U0126 (Cell Signaling).

    Techniques:

    N2A-1B control cells, β-arrestin 1 KO cells (β-Arr1 KO), and β-arrestin 2 KO cells (β-Arr2 KO) received treatment with the 5-HT1B agonist CP-94253 (100 nM) alone or pretreatment with the 5-HT1B antagonist SB-224289 (1 μM) 1 hour prior to agonist treatment and compared to unstimulated control cells treated with vehicle (PBS). (a) Levels of phospho-ERK1 significantly differed by treatment (F2,36 = 21.4, p < 0.0001) and cell type (F2,36 = 4.79, p = 0.014), with a significant interaction between treatment and cell type (F4,36 = 7.017, p < 0.001). 5-HT1B receptor stimulation with agonist significantly increased levels of phospho-ERK1 in control cells (p < 0.0001) but not in β-Arr1 KO (p = 0.918) or β-Arr2 KO cells (p = 0.997). (b) Levels of phospho-ERK2 also significantly differed by treatment (F2,36 = 19.3, p < 0.0001) and cell type (F2,36 = 4.362, p = 0.020), with a significant interaction between treatment and cell type (F4,36 = 4.469, p = 0.049). 5-HT1B receptor stimulation significantly increased levels of phospho-ERK2 in control cells (p = 0.0003) but not in β-Arr1 KO (p = 0.917) or β-Arr2 KO cells (p = 0.680). Furthermore, SB-224289 blocks agonist-induced ERK1/2 activation, reducing phospho-ERK1 levels in control (p = 0.045) and β-Arr2 KO cells (p = 0.043) (a) and reducing phospho-ERK2 levels in control (p = 0.048) and β-Arr1 KO cells (p = 0.014) (b). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 5 independent biological replicates for all groups (two-way ANOVA with Dunnett’s post hoc tests; ***p < 0.001, *p < 0.05).

    Journal: ACS chemical neuroscience

    Article Title: 5-HT 1B RECEPTOR-MEDIATED ACTIVATION OF ERK1/2 REQUIRES BOTH Gα i/o AND β-ARRESTIN PROTEINS

    doi: 10.1021/acschemneuro.8b00596

    Figure Lengend Snippet: N2A-1B control cells, β-arrestin 1 KO cells (β-Arr1 KO), and β-arrestin 2 KO cells (β-Arr2 KO) received treatment with the 5-HT1B agonist CP-94253 (100 nM) alone or pretreatment with the 5-HT1B antagonist SB-224289 (1 μM) 1 hour prior to agonist treatment and compared to unstimulated control cells treated with vehicle (PBS). (a) Levels of phospho-ERK1 significantly differed by treatment (F2,36 = 21.4, p < 0.0001) and cell type (F2,36 = 4.79, p = 0.014), with a significant interaction between treatment and cell type (F4,36 = 7.017, p < 0.001). 5-HT1B receptor stimulation with agonist significantly increased levels of phospho-ERK1 in control cells (p < 0.0001) but not in β-Arr1 KO (p = 0.918) or β-Arr2 KO cells (p = 0.997). (b) Levels of phospho-ERK2 also significantly differed by treatment (F2,36 = 19.3, p < 0.0001) and cell type (F2,36 = 4.362, p = 0.020), with a significant interaction between treatment and cell type (F4,36 = 4.469, p = 0.049). 5-HT1B receptor stimulation significantly increased levels of phospho-ERK2 in control cells (p = 0.0003) but not in β-Arr1 KO (p = 0.917) or β-Arr2 KO cells (p = 0.680). Furthermore, SB-224289 blocks agonist-induced ERK1/2 activation, reducing phospho-ERK1 levels in control (p = 0.045) and β-Arr2 KO cells (p = 0.043) (a) and reducing phospho-ERK2 levels in control (p = 0.048) and β-Arr1 KO cells (p = 0.014) (b). Data are expressed as the percent change in pERK signal compared to the no agonist control from each independent biological replicate. Error bars represent SEM and data are averages of 5 independent biological replicates for all groups (two-way ANOVA with Dunnett’s post hoc tests; ***p < 0.001, *p < 0.05).

    Article Snippet: Treatment drugs used were: CP-94253, 56 SB-224289, 53 , gallein (Tocris), pertussis toxin (Novex), and U0126 (Cell Signaling).

    Techniques: Activation Assay

    Effects of RU 24969 (left) and CP 94253 (right) at various doses on PS in 5-HT1B+/+ (open symbols) and 5-HT1B−/− (filled symbols) mice during the 4 hr after injection in which an effect was observed. Results are expressed as minutes (mean ± SEM of 8 mice in each group for RU 24969 and 6 mice for CP 94253; 5–8 tests for each dose). *p < 0.05, significantly different from baseline (0 on abscissa); paired Student’st test. Complete set of data is available on request.

    Journal: The Journal of Neuroscience

    Article Title: Key Role of 5-HT 1B Receptors in the Regulation of Paradoxical Sleep as Evidenced in 5-HT 1B Knock-Out Mice

    doi: 10.1523/JNEUROSCI.19-08-03204.1999

    Figure Lengend Snippet: Effects of RU 24969 (left) and CP 94253 (right) at various doses on PS in 5-HT1B+/+ (open symbols) and 5-HT1B−/− (filled symbols) mice during the 4 hr after injection in which an effect was observed. Results are expressed as minutes (mean ± SEM of 8 mice in each group for RU 24969 and 6 mice for CP 94253; 5–8 tests for each dose). *p < 0.05, significantly different from baseline (0 on abscissa); paired Student’st test. Complete set of data is available on request.

    Article Snippet: Chemicals RU 24969 (0.25–5.0 mg/kg, i.p.) was obtained from Roussel-Uclaf (Romainville, France); WAY 100635 (0.05–1.0 mg/kg, i.p.) was from Wyeth Research (Princeton, NJ); 8-OH-DPAT (0.2–1.2 mg/kg, s.c.) was obtained from Research Biochemicals (Natick, MA); CP 94253 (1.0–10.0 mg/kg, i.p.) was from Pfizer Central Research (Groton, CT); and GR 127935 (0.1–1.0 mg/kg, i.p.) was from Glaxo-Wellcome (Ware, UK).

    Techniques: Injection

    Effects of the 5-HT 1B agonist  CP 94253  at various doses on sleep and wakefulness in 5-HT 1B +/+ and 5-HT 1B −/− mice during the 4 hr after injection

    Journal: The Journal of Neuroscience

    Article Title: Key Role of 5-HT 1B Receptors in the Regulation of Paradoxical Sleep as Evidenced in 5-HT 1B Knock-Out Mice

    doi: 10.1523/JNEUROSCI.19-08-03204.1999

    Figure Lengend Snippet: Effects of the 5-HT 1B agonist CP 94253 at various doses on sleep and wakefulness in 5-HT 1B +/+ and 5-HT 1B −/− mice during the 4 hr after injection

    Article Snippet: Chemicals RU 24969 (0.25–5.0 mg/kg, i.p.) was obtained from Roussel-Uclaf (Romainville, France); WAY 100635 (0.05–1.0 mg/kg, i.p.) was from Wyeth Research (Princeton, NJ); 8-OH-DPAT (0.2–1.2 mg/kg, s.c.) was obtained from Research Biochemicals (Natick, MA); CP 94253 (1.0–10.0 mg/kg, i.p.) was from Pfizer Central Research (Groton, CT); and GR 127935 (0.1–1.0 mg/kg, i.p.) was from Glaxo-Wellcome (Ware, UK).

    Techniques: Injection

    Effects of the 5-HT1B/1D antagonist GR 127935 (hatched bars) on PS inhibition induced by RU 24969 (gray bars) or CP 94253 (black bars) in 5-HT1B+/+ mice during the 2 hr period after injection in which an effect was observed. Results are expressed as minutes (mean ± SEM of 8 animals; 8 and 6 tests for each treatment, respectively). *p < 0.05, significantly different from baseline (open bar); paired Student’st test. Complete set of data is available on request.

    Journal: The Journal of Neuroscience

    Article Title: Key Role of 5-HT 1B Receptors in the Regulation of Paradoxical Sleep as Evidenced in 5-HT 1B Knock-Out Mice

    doi: 10.1523/JNEUROSCI.19-08-03204.1999

    Figure Lengend Snippet: Effects of the 5-HT1B/1D antagonist GR 127935 (hatched bars) on PS inhibition induced by RU 24969 (gray bars) or CP 94253 (black bars) in 5-HT1B+/+ mice during the 2 hr period after injection in which an effect was observed. Results are expressed as minutes (mean ± SEM of 8 animals; 8 and 6 tests for each treatment, respectively). *p < 0.05, significantly different from baseline (open bar); paired Student’st test. Complete set of data is available on request.

    Article Snippet: Chemicals RU 24969 (0.25–5.0 mg/kg, i.p.) was obtained from Roussel-Uclaf (Romainville, France); WAY 100635 (0.05–1.0 mg/kg, i.p.) was from Wyeth Research (Princeton, NJ); 8-OH-DPAT (0.2–1.2 mg/kg, s.c.) was obtained from Research Biochemicals (Natick, MA); CP 94253 (1.0–10.0 mg/kg, i.p.) was from Pfizer Central Research (Groton, CT); and GR 127935 (0.1–1.0 mg/kg, i.p.) was from Glaxo-Wellcome (Ware, UK).

    Techniques: Inhibition, Injection

    Cylinder test is a well-established spontaneous motor test based on limb-use asymmetry known to be sensitive to graft-induced functional recovery (A). All animals were severely impaired in the use of left forelimb (contralateral to the lesion side, open bars in A). 5HT grafts were functionally ineffective, whereas DA grafts ameliorated the limb use deficit significantly at 12 weeks after grafting (Two-way ANOVA F (5,163) = 16.75, p<0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0083). The animals were then challenged with L-DOPA to assess if the grafts were able to modulate the dyskinesia that were established prior to transplantation (B; two-way ANOVA F (8,245) = 63.48, p = <0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0033). DA-cell rich grafts reduced the dyskinesia, while 5HT cells were ineffective or even aggravated the dyskinesia. Co-treatment of the animals with 5HT receptor 1A and 1B agonists (0.1 mg/kg 8-OH-DPAT and 1.75 mg/kg CP-94253) reduced the dyskinesia significantly in all groups (B). The residual abnormal movements were primarily due to differential duration of action of L-DOPA and the agonists (C). tx: transplantation, *: different from pre-tx baseline; +: different from post-tx 12 wks; #: different from 6OHDA lesion and 5HT groups.

    Journal: PLoS ONE

    Article Title: Differential Dopamine Receptor Occupancy Underlies L-DOPA-Induced Dyskinesia in a Rat Model of Parkinson's Disease

    doi: 10.1371/journal.pone.0090759

    Figure Lengend Snippet: Cylinder test is a well-established spontaneous motor test based on limb-use asymmetry known to be sensitive to graft-induced functional recovery (A). All animals were severely impaired in the use of left forelimb (contralateral to the lesion side, open bars in A). 5HT grafts were functionally ineffective, whereas DA grafts ameliorated the limb use deficit significantly at 12 weeks after grafting (Two-way ANOVA F (5,163) = 16.75, p<0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0083). The animals were then challenged with L-DOPA to assess if the grafts were able to modulate the dyskinesia that were established prior to transplantation (B; two-way ANOVA F (8,245) = 63.48, p = <0.001; followed by pairwise comparison adjusted using Bonferroni, p<0.0033). DA-cell rich grafts reduced the dyskinesia, while 5HT cells were ineffective or even aggravated the dyskinesia. Co-treatment of the animals with 5HT receptor 1A and 1B agonists (0.1 mg/kg 8-OH-DPAT and 1.75 mg/kg CP-94253) reduced the dyskinesia significantly in all groups (B). The residual abnormal movements were primarily due to differential duration of action of L-DOPA and the agonists (C). tx: transplantation, *: different from pre-tx baseline; +: different from post-tx 12 wks; #: different from 6OHDA lesion and 5HT groups.

    Article Snippet: To evaluate the effect of the 5HT receptor agonists on L-DOPA induced dyskinesia, selective 5-HT1A agonist, 8-OH-DPAT ((±)-8-hydroxy-2-dipropylaminotetralin hydrobromide; TOCRIS, Sweden), and the 5-HT1B agonist, CP-94253 (TOCRIS, Sweden) were injected subcutaneously 5 min before L-DOPA.

    Techniques: Functional Assay, Comparison, Transplantation Assay