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Coulbourn Instruments standard operant chambers
Standard Operant Chambers, supplied by Coulbourn Instruments, 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/product/standard+operant+chambers/chambers+operant/pmc13211988-87-18-29
Average 86 stars, based on 1 article reviews
standard operant chambers - by Bioz Stars, 2026-10
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Article Title: Effects of reproductive experience on cost-benefit decision making in female rats
Article Snippet: Behavioral testing was conducted in eight standard operant chambers (Coulbourn Instruments).

Article Title: A novel cost-benefit decision-making task involving cued punishment; effects of sex and psychostimulant administration
Article Snippet: Behavioral testing was conducted in standard operant chambers (Coulbourn Instruments).

Article Title: Propensity for risky choices despite lower cue reactivity in adolescent rats
Article Snippet: Behavioral training and testing took place in 8 standard operant chambers (Coulbourn Instruments) equipped with a house light, food magazine, and three illuminable nosepoke operanda recessed into the wall opposite the food magazine.

Article Title: Assessment of Cell-Type-Specific Excitatory Synaptic Strength in the Dorsolateral Striatum of Goal-Directed and Habitual Cocaine-Seeking Behavior
Article Snippet: The cocaine self-administration paradigm, adapted from and , was performed during the light cycle and conducted in eight standard operant chambers that were enclosed in sound- and light-attenuating cabinets (Coulbourn Instruments).

Article Title: Effects of fentanyl self-administration on risk-taking behavior in male rats
Article Snippet: Apparatus Self-administration occurred in standard operant chambers (Coulbourn Instruments; 12 chambers, UF; 9 chambers, UT Austin) housed in sound-attenuating cabinets.

Article Title: Effects of systemic oxytocin receptor activation and blockade on risky decision making in female and male rats.
Article Snippet: Behavioral testing was conducted in eight standard operant chambers (Coulbourn Instruments).

Article Title: Effects of fentanyl self-administration on risk-taking behavior in male rats
Article Snippet: The other behavioral tasks were also conducted in standard operant chambers (Coulbourn Instruments; 12 chambers, UF; 10 chambers, UT Austin) housed in sound-attenuating cabinets and located in a different room than that used for self-administration.



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Med Associates Inc standard mouse operant conditioning chamber
MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear <t>conditioning.</t> Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.
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Coulbourn Instruments soundattenuating standard operant chamber
MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear <t>conditioning.</t> Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.
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Med Associates Inc apparatus standard operant chambers
MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear <t>conditioning.</t> Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.
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Med Associates Inc identical standard twin lever operant chambers
MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear <t>conditioning.</t> Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.
Identical Standard Twin Lever Operant Chambers, supplied by Med Associates Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear conditioning. Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.

Journal: iScience

Article Title: Melanocortin 4 receptor-expressing neurons in the lateral stripe of the striatum regulate affect and motor control

doi: 10.1016/j.isci.2025.112456

Figure Lengend Snippet: MC4R-LSS neurons are activated by aversive foot shocks in a D1-independent manner (A) Timeline of experiments. (B) Representative picture of GCaMP8m-expression and fiber placement in the lateral stripe of the striatum (LSS) of an MC4R-cre mouse. Fiber tract and anterior commissure (aca) marked with dashed line; LSS marked with arrow. LV, lateral ventricle. Scale bar 200 μm. (C) GCaMP8m signal measured with fiber photometry from MC4R-LSS neurons shows activation of MC4R-LSS neurons in response to aversive shocks, but not to the onset of the predictive tone cue. No change in neural activity was seen in response to shock omission in the fear test on day 2. Mean and SEM from 6 mice, 6 trials per mouse. (D) Heatmap of the data shown in (C) but split out per trial showing that the neural response is similar across all trials. Each row in the heatmap represents the mean from 6 mice. (E) Dopamine measurements from the LSS during the same behavioral paradigm as in (C). Dopamine is released in the LSS in response to both the aversive foot shocks and their predictive tone cues. No clear change in dopamine release was seen in response to shock omission in the fear test on day 2. Mean and SEM from 7 mice, 6 trials per mouse. (F) Heatmap of the data shown in (E) but split out per trial showing that the tone-induced dopamine release develops during the session. Each row in the heatmap represents the mean from 7 mice. (G) iGluSnFR-measurements of glutamate release onto D1-expressing neurons in the LSS during fear conditioning. Glutamate is released onto D1-expressing neurons in response to the aversive foot shock. A small release can be seen in response to the tone onset. Mean and SEM from 10 mice, 6 trials per mouse. (H) Heatmap of the data shown in (G), but split out per trial, showing that the shock-induced glutamate release is similar across trials and that the tone-induced release is developed within the session. Each row in the heatmap represents the mean from 10 mice. (I) Timeline of the crossover experiment testing if shock-induced activity of MC4R-LSS neurons is D1-dependent. (J) Group mean peri-event traces (± SEM) from the experiment shows a robust increase in neural activity in response to the foot shock after both saline-injection and pretreatment with the D1-antagonist SCH23390 (0.2 mg/kg; n = 7). (K) Mean peak size during the shock for each animal showing that SCH23390 does not affect the shock-induced neural response ( n = 7, paired two-tailed t-test). (L) Analysis of the inactivity time during the sessions showing that mice spend significantly more time inactive after SCH23390 injection compared to saline injection ( n = 11, paired two-tailed t-test). ∗∗∗ p < 0.001.

Article Snippet: Standard mouse operant conditioning chamber , Med Associates , ENV-307W.

Techniques: Expressing, Activation Assay, Activity Assay, Saline, Injection, Two Tailed Test