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cp945598 hydrochloride  (Tocris)


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    Tocris cp945598 hydrochloride
    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.
    Cp945598 Hydrochloride, supplied by Tocris, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 91 stars, based on 2 article reviews
    cp945598 hydrochloride - by Bioz Stars, 2026-07
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    Images

    1) Product Images from "Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons"

    Article Title: Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons

    Journal: eLife

    doi: 10.7554/eLife.33892

    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.
    Figure Legend Snippet: ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.

    Techniques Used: Blocking Assay, Activity Assay, Transmission Assay

    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R antagonist CP945598. Right: summary data for EPSC amplitude over time, normalized to baseline. n = 6 neurons from four mice. ( B ) Summary results show paired-pulse ratio during baseline and following CB1R agonist WIN55212-2 application and oxytocin application in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, and orlistat (THL), separately. **p<0.01, Wilcoxon matched-pairs signed rank test. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and six neurons from four mice. Error bars reflect SEM.
    Figure Legend Snippet: ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R antagonist CP945598. Right: summary data for EPSC amplitude over time, normalized to baseline. n = 6 neurons from four mice. ( B ) Summary results show paired-pulse ratio during baseline and following CB1R agonist WIN55212-2 application and oxytocin application in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, and orlistat (THL), separately. **p<0.01, Wilcoxon matched-pairs signed rank test. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and six neurons from four mice. Error bars reflect SEM.

    Techniques Used:


    Figure Legend Snippet:

    Techniques Used: Concentration Assay, Recombinant, RNAscope, Fluorescence, Multiplex Assay, Software



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    Tocris cp945598 hydrochloride
    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.
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    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page
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    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page
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    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page
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    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page
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    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist <t>CP945598,</t> orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page
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    Image Search Results


    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.

    Journal: eLife

    Article Title: Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons

    doi: 10.7554/eLife.33892

    Figure Lengend Snippet: ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 μM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. ( B ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. ( C ) Same as ( B ), but in the presence of CB1R inverse agonist AM251. ( D ) Same as ( B ), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase α (DGLα). ( E ) Same as ( B ), but with THL in the internal solution to block 2-AG synthesis. ( F ) Same as ( B ), but with U73122 in the internal solution to inhibit PLC activity. ( G ) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank test vs. baseline. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and seven neurons from four mice. Error bars reflect SEM. ( H ) Schematic summary of the mechanism underlying direct oxytocinergic regulation of excitatory synaptic transmission in VTA DA neurons. Oxytocin binds to G q -coupled OxtR, activating the phospholipase C (PLC) pathway. PLC cleaves phosphatidylinositol 1,4,5-bisphosphate into diacylglycerol (DAG) and inositol 1,4,5-trisphosphate, and DAG is subsequently converted into 2-AG by DAG lipase (DGL). 2-AG released by VTA DA neurons binds to presynaptic G i/o -coupled CB1R, decreasing glutamate release. 10.7554/eLife.33892.013 Figure 3—source data 1. Summary tables of evoked EPSC amplitudes in response to endocannabinoid-signaling related pharmacological agents.

    Article Snippet: chemical compound, drug , CP945598 hydrochloride , Tocris , Cat#4236; CAS 686347-12-6 , .

    Techniques: Blocking Assay, Activity Assay, Transmission Assay

    ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R antagonist CP945598. Right: summary data for EPSC amplitude over time, normalized to baseline. n = 6 neurons from four mice. ( B ) Summary results show paired-pulse ratio during baseline and following CB1R agonist WIN55212-2 application and oxytocin application in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, and orlistat (THL), separately. **p<0.01, Wilcoxon matched-pairs signed rank test. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and six neurons from four mice. Error bars reflect SEM.

    Journal: eLife

    Article Title: Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons

    doi: 10.7554/eLife.33892

    Figure Lengend Snippet: ( A ) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 μM oxytocin application in the presence of CB1R antagonist CP945598. Right: summary data for EPSC amplitude over time, normalized to baseline. n = 6 neurons from four mice. ( B ) Summary results show paired-pulse ratio during baseline and following CB1R agonist WIN55212-2 application and oxytocin application in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, and orlistat (THL), separately. **p<0.01, Wilcoxon matched-pairs signed rank test. For each condition respectively, n = 7 neurons from five mice, six neurons from four mice, six neurons from three mice, six neurons from four mice, six neurons from four mice, seven neurons from four mice, and six neurons from four mice. Error bars reflect SEM.

    Article Snippet: chemical compound, drug , CP945598 hydrochloride , Tocris , Cat#4236; CAS 686347-12-6 , .

    Techniques:

    Journal: eLife

    Article Title: Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons

    doi: 10.7554/eLife.33892

    Figure Lengend Snippet:

    Article Snippet: chemical compound, drug , CP945598 hydrochloride , Tocris , Cat#4236; CAS 686347-12-6 , .

    Techniques: Concentration Assay, Recombinant, RNAscope, Fluorescence, Multiplex Assay, Software

    Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page

    Journal: eLife

    Article Title: Oxytocin functions as a spatiotemporal filter for excitatory synaptic inputs to VTA dopamine neurons

    doi: 10.7554/elife.33892

    Figure Lengend Snippet: Figure 3. Retrograde endocannabinoid signaling underlies oxytocinergic modulation of excitatory synaptic transmission. (A) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 5 mM CB1R agonist WIN55212-2 application. Right: summary data for EPSC amplitude over time, normalized to baseline. (B) Left: example traces of evoked EPSCs from one VTA DA neuron during baseline and following 1 mM oxytocin application in the presence of CB1R agonist WIN55212-2. Right: summary data for EPSC amplitude over time, normalized to baseline. (C) Same as (B), but in the presence of CB1R inverse agonist AM251. (D) Same as (B), but in the presence of orlistat (THL), a blocker of 2-AG synthesizing enzyme diacylglycerol lipase a (DGLa). (E) Same as (B), but with THL in the internal solution to block 2-AG synthesis. (F) Same as (B), but with U73122 in the internal solution to inhibit PLC activity. (G) Summary data for EPSC amplitude changes induced by CB1R agonist WIN55212-2 and oxytocin in the presence of WIN55212-2, CB1R inverse agonist AM251, CB1R antagonist CP945598, orlistat (THL), intracellular THL, and intracellular U73122, separately. **p<0.01, Wilcoxon signed rank Figure 3 continued on next page

    Article Snippet: DOI: https://doi.org/10.7554/eLife.33892 17 of 26 Continued Reagent type (species) or resource Designation Source or reference Identifiers Additional information chemical compound, drug SR 49059 Tocris Cat#2310; CAS 150375-75-0 chemical compound, drug NBQX disodium salt Tocris Cat#1044; CAS 479347-86-9 chemical compound, drug (RS)-CPP Tocris Cat#0173; CAS 100828-16-8 chemical compound, drug SR95531 hydrobromide Tocris Cat#1262; CAS 104104-50-9 chemical compound, drug U73122 Tocris Cat#1268; CAS 112648-68-7 chemical compound, drug CP945598 hydrochloride Tocris Cat#4236; CAS 686347-12-6 chemical compound, drug WIN55212-2 Tocris Cat#1038; CAS 131543-23-2 chemical compound, drug AM251 Tocris Cat#1117; CAS 183232-66-8 chemical compound, drug orlistat (THL) Tocris Cat#3540; CAS 96829-58-2 chemical compound, drug MNI-L-glutamate Tocris Cat#1490; CAS 295325-62-1 chemical compound, drug Alexa Fluor 488 hydrazide Thermo Fisher Scientific Cat#A10436 chemical compound, drug Alexa Fluor 594 hydrazide Thermo Fisher Scientific Cat#A10438 chemical compound, drug Green retrobeads (GRB) Lumafluor Inc. Cat#G180 software, algorithm GraphPad Prizm 5 GraphPad RRID:SCR_002798 software, algorithm FIJI Schindelin et al., 2012 http://fiji.sc/; RRID:SCR_002285 software, algorithm MATLAB MathWorks RRID:SCR_001622 software, algorithm Igor Pro Wavemetrics RRID:SCR_000325 software, algorithm SPSS IBM RRID:SCR_002865

    Techniques: Transmission Assay, Blocking Assay, Activity Assay