5 hydroxytryptamine hydrochloride  (Alomone Labs)


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    Alomone Labs 5 hydroxytryptamine hydrochloride
    <t>5-HT</t> inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    5 Hydroxytryptamine Hydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey"

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-4-54

    5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    Figure Legend Snippet: 5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.

    Techniques Used: Concentration Assay, Produced

    5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.
    Figure Legend Snippet: 5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.

    Techniques Used: Activation Assay, Inhibition, Produced

    5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.
    Figure Legend Snippet: 5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.

    Techniques Used: Inhibition, Produced, Incubation

    5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.
    Figure Legend Snippet: 5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.

    Techniques Used:

    5 hydroxytryptamine hydrochloride  (Alomone Labs)


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  • 94

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    Alomone Labs 5 hydroxytryptamine hydrochloride
    <t>5-HT</t> inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    5 Hydroxytryptamine Hydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/5 hydroxytryptamine hydrochloride/product/Alomone Labs
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    94/100 stars

    Images

    1) Product Images from "Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey"

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    Journal: Molecular Pain

    doi: 10.1186/1744-8069-4-54

    5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    Figure Legend Snippet: 5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.

    Techniques Used: Concentration Assay, Produced

    5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.
    Figure Legend Snippet: 5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.

    Techniques Used: Activation Assay, Inhibition, Produced

    5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.
    Figure Legend Snippet: 5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.

    Techniques Used: Inhibition, Produced, Incubation

    5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.
    Figure Legend Snippet: 5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.

    Techniques Used:

    n m recombinant basic fibroblast growth factor  (Alomone Labs)


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    Alomone Labs n m recombinant basic fibroblast growth factor
    N M Recombinant Basic Fibroblast Growth Factor, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    5 hydroxytryptamine  (Alomone Labs)


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    Alomone Labs 5 hydroxytryptamine
    Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, <t>Similarly,</t> <t>5-HT</t> (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).
    5 Hydroxytryptamine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/5 hydroxytryptamine/product/Alomone Labs
    Average 94 stars, based on 1 article reviews
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    1) Product Images from "Physiological Role of Calcium-Activated Potassium Currents in the Rat Lateral Amygdala"

    Article Title: Physiological Role of Calcium-Activated Potassium Currents in the Rat Lateral Amygdala

    Journal: The Journal of Neuroscience

    doi: 10.1523/JNEUROSCI.22-05-01618.2002

    Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, Similarly, 5-HT (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).
    Figure Legend Snippet: Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, Similarly, 5-HT (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).

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    Alomone Labs 5 hydroxytryptamine hydrochloride
    <t>5-HT</t> inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    5 Hydroxytryptamine Hydrochloride, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Alomone Labs n m recombinant basic fibroblast growth factor
    <t>5-HT</t> inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.
    N M Recombinant Basic Fibroblast Growth Factor, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/n m recombinant basic fibroblast growth factor/product/Alomone Labs
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    Alomone Labs 5 hydroxytryptamine
    Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, <t>Similarly,</t> <t>5-HT</t> (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).
    5 Hydroxytryptamine, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/5 hydroxytryptamine/product/Alomone Labs
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    5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.

    Journal: Molecular Pain

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    doi: 10.1186/1744-8069-4-54

    Figure Lengend Snippet: 5-HT inhibits evoked IPSCs in PAG neurons . (A) Time course of evoked IPSC amplitude (eIPSC Ampl) during application of 5-HT (10 μM), baclofen (10 μM) and CGP55845 (CGP, 1 μM). (B) Averaged evoked IPSCs before (control) and during application of 5-HT and baclofen. (C) Averaged evoked IPSCs in response to identical paired stimuli (inter-stimulus interval = 70 ms) for the traces in B, with IPSC 1 normalized to demonstrate relative facilitation of IPSC 2 during superfusion of 5-HT. (D) Concentration-response curve of the reduction in evoked IPSC (eIPSC) amplitude produced by 5-HT, expressed as a percentage of the pre-5-HT level, with a logistic function fitted to determine the IC 50 . (E) Bar chart showing the amplitude of the first evoked IPSC (eIPSC1) and the ratio of evoked IPSC 2 /IPSC 1 (eIPSC2:1) in the presence of 5-HT (10 μM), fluoxetine (30 μM) and baclofen (10 μM), expressed as a percentage of the pre-drug level. In (D) *, ** and ## denote p < 0.05, 0.01 and 0.0001. Traces in (A – C) are from the same neuron.

    Article Snippet: BRL15572 hydrochloride, CP93129, fluoxetine hydrochloride, L694247, LY344864, NAS-181, (2R)-(+)-8-Hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), SR95531 hydrobromide and (S)-WAY100135 dihydrochloride were obtained from Tocris Cookson (Bristol, UK); QX-314 bromide and TTX from Alomone Laboratories (Jerusalem, Israel); 6-cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX), 5-hydroxytryptamine hydrochloride (5-HT), and strychnine hydrochloride from Sigma (Sydney, Australia).

    Techniques: Concentration Assay, Produced

    5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.

    Journal: Molecular Pain

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    doi: 10.1186/1744-8069-4-54

    Figure Lengend Snippet: 5-HT1A, 5-HT1B and 5-HT1D receptor activation inhibits evoked IPSCs in PAG neurons . Averaged evoked IPSCs are shown prior to (control) and during (agonist) addition of (A) the 5-HT1A agonist 8-OH-DPAT (3 μM), (B) the 5-HT1B agonist CP93129 (3 μM), (C) the 5-HT1D agonist L694247 (3 μM) and (D) the 5-HT1F agonist LY344864 (3 μM). (E) Bar chart showing the percentage inhibition of evoked IPSC amplitude (eIPSC Ampl) produced by 5-HT (1 μM), 8-OH-DPAT (3 μM), CP93129 (3 μM) L694247 (3 μM) and LY344864 (1 – 3 μM) expressed as a percentage of the pre-drug level. In (E), *, **, # and ## denote p < 0.05, 0.01, 0.001 and 0.0001. Traces in (A – D) are from different neurons, bars are 200 pA and 10 ms.

    Article Snippet: BRL15572 hydrochloride, CP93129, fluoxetine hydrochloride, L694247, LY344864, NAS-181, (2R)-(+)-8-Hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), SR95531 hydrobromide and (S)-WAY100135 dihydrochloride were obtained from Tocris Cookson (Bristol, UK); QX-314 bromide and TTX from Alomone Laboratories (Jerusalem, Israel); 6-cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX), 5-hydroxytryptamine hydrochloride (5-HT), and strychnine hydrochloride from Sigma (Sydney, Australia).

    Techniques: Activation Assay, Inhibition, Produced

    5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.

    Journal: Molecular Pain

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    doi: 10.1186/1744-8069-4-54

    Figure Lengend Snippet: 5-HT inhibition of evoked IPSCs is largely mediated by 5-HT1B receptors . Bar chart displaying the mean reduction in evoked IPSC amplitude produced by 5-HT (1 μM) in neurons which were either not pre-incubated in any antagonist (control), or were pre-incubated in the 5-HT1A antagonist WAY100135 (3 μM), the 5-HT1B antagonist NAS181 (10 μM), or the 5-HT1D antagonist BRL15572 (10 μM). Evoked IPSC amplitude is expressed as a percentage of the pre-5-HT level. **, ## denote p < 0.01, 0.0001.

    Article Snippet: BRL15572 hydrochloride, CP93129, fluoxetine hydrochloride, L694247, LY344864, NAS-181, (2R)-(+)-8-Hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), SR95531 hydrobromide and (S)-WAY100135 dihydrochloride were obtained from Tocris Cookson (Bristol, UK); QX-314 bromide and TTX from Alomone Laboratories (Jerusalem, Israel); 6-cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX), 5-hydroxytryptamine hydrochloride (5-HT), and strychnine hydrochloride from Sigma (Sydney, Australia).

    Techniques: Inhibition, Produced, Incubation

    5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.

    Journal: Molecular Pain

    Article Title: Sumatriptan inhibits synaptic transmission in the rat midbrain periaqueductal grey

    doi: 10.1186/1744-8069-4-54

    Figure Lengend Snippet: 5-HT inhibits evoked EPSCs in PAG neurons . (A) Time course of evoked EPSC amplitude (eEPSC Ampl) during application of 5-HT (10 μM) and sumatriptan (3 μM). (B) Averaged evoked EPSCs before (control) and during application of 5-HT and sumatriptan. (C) Bar chart showing the amplitude of the first evoked EPSC (eEPSC1) and the ratio of evoked EPSC 2 /EPSC 1 (eEPSC2:1) in the presence of 5-HT (10 μM) and sumatriptan (3 μM), expressed as a percentage of the pre-drug level. In (C) * and ## denote p < 0.05 and 0.0001. Traces in (A – B) are from the same neuron.

    Article Snippet: BRL15572 hydrochloride, CP93129, fluoxetine hydrochloride, L694247, LY344864, NAS-181, (2R)-(+)-8-Hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), SR95531 hydrobromide and (S)-WAY100135 dihydrochloride were obtained from Tocris Cookson (Bristol, UK); QX-314 bromide and TTX from Alomone Laboratories (Jerusalem, Israel); 6-cyano-7-nitroquinoxaline-2,3-dione disodium (CNQX), 5-hydroxytryptamine hydrochloride (5-HT), and strychnine hydrochloride from Sigma (Sydney, Australia).

    Techniques:

    Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, Similarly, 5-HT (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).

    Journal: The Journal of Neuroscience

    Article Title: Physiological Role of Calcium-Activated Potassium Currents in the Rat Lateral Amygdala

    doi: 10.1523/JNEUROSCI.22-05-01618.2002

    Figure Lengend Snippet: Neurotransmitters modulate the slow AHP and reduce spike-frequency adaptation. A1, Application of carbachol (20 μm) depressed the slow AHP but not the medium AHP in an atropine-sensitive manner. A2, This was accompanied by a reduction in spike-frequency adaptation, which was reversed by atropine (1 μm). B1, In the presence of noradrenaline (10 μm), the slow AHP was blocked and was replaced with a slow afterdepolarization. B2, In voltage clamp, noradrenaline selectively blocked the sIAHP, evoking an inward current. B3, This caused a concurrent reduction in accommodation. C, Similarly, 5-HT (10 μm) selectively blocked the slow AHP (C1) and sIAHP (C2), which caused a decrease in spike-frequency adaptation (C3).

    Article Snippet: Ibtx, α-dendrotoxin (DTX), and apamin were obtained from Alomone Laboratories (Jerusalem, Israel); nickel, cadmium, EGTA, BAPTA, carbachol, isoprenaline, paxilline, tetraethylammonium (TEA), atropine, noradrenaline, dopamine, 5-hydroxytryptamine (5-HT), muscarine, and 4-aminopyridine (4-AP) were obtained from Sigma (St. Louis, MO).

    Techniques: