Evidence that the reward attenuating effect of the D1-like antagonist, SCH-23390, is not mediated by its agonist action at the 5-HT2c receptors

Benaliouad, Faïza; Zhornitsky, Simon; Rompré, Pierre‐Paul

doi:10.1016/j.bbr.2010.09.023

Cited by 5 publications

(10 citation statements)

References 25 publications

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“…Likewise, SB242084 blocked the ability of lorcaserin to lower maximum response rates (Figure B, D; lorcaserin × SB242084: F 1,20 = 33.975, p < 0.001; lorcaserin × SB242084 × site: F 1,20 = 0.075, NS; lorcaserin × SB242084 × pass × site: F 3,60 = 0.947, NS). When administered without lorcaserin present, SB242084 minimally affected the M50 or maximum response rates, similar to previous studies. , These data confirm that the ability of lorcaserin to both increase thresholds and decrease maximum response rates is mediated through activation of 5-HT 2C receptors.…”

Section: Results and Discussionsupporting

confidence: 89%

“…When administered without lorcaserin present, SB242084 minimally affected the M50 or maximum response rates, similar to previous studies. 48,50 These data confirm that the ability of lorcaserin to both increase thresholds and decrease maximum response rates is mediated through activation of 5-HT 2C receptors. During Current Training, the minimum current required to maintain a response rate that delivered 40 rewards per trial at a set frequency of 141 Hz (A) was similar for rats with electrodes in the MFB or DRN (B).…”

Section: ■ Results and Discussionsupporting

confidence: 71%

“…For Experiments 1A and 1B, following an injection, the M50 for each pass was analyzed as a percent of each daily baseline, similar to previous reports. , Maximum response rates were not converted to a percentage as there was a clear difference in response rates between the MFB and DRN groups. These values, as well as the maximum response rate, were analyzed using a repeated measures ANOVA with Session as a within-subjects factor and Site as a between-subjects factor, as well as for animals in each group separately.…”

Section: Methodsmentioning

confidence: 99%

“…In contrast, increased reward thresholds were observed following systemic administration of a nonselective 5-HT 2C agonist, TFMPP, or more selective 5-HT 2C agonists, WAY 161503 or CP 809101. − Therefore, 5-HT 2C receptor agonists can decrease the efficacy of BSR. An important objective of the present study is to determine whether lorcaserin, like other 5-HT 2C receptor agonists, likewise decreases the efficacy of BSR (i.e., increases reward thresholds).…”

mentioning

confidence: 99%

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The Serotonin 2C Receptor Agonist Lorcaserin Attenuates Intracranial Self-Stimulation and Blocks the Reward-Enhancing Effects of Nicotine

Zeeb

Higgins

Fletcher

2015

ACS Chem. Neurosci.

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Lorcaserin, a serotonin (5-hydroxytryptamine, 5-HT) 2C receptor agonist, was recently approved for the treatment of obesity. We previously suggested that 5-HT2C receptor agonists affect reward processes and reduce the rewarding effects of drugs of abuse. Here, we determined whether lorcaserin (1) decreases responding for brain stimulation reward (BSR) and (2) prevents nicotine from enhancing the efficacy of BSR. Rats were trained on the intracranial self-stimulation (ICSS) paradigm to nosepoke for BSR of either the dorsal raphé nucleus or left medial forebrain bundle. In Experiment 1, lorcaserin (0.3-1.0 mg/kg) dose-dependently reduced the efficacy of BSR. This effect was blocked by prior administration of the 5-HT2C receptor antagonist SB242084. In Experiment 2, separate groups of rats received saline or nicotine (0.4 mg/kg) for eight sessions prior to testing. Although thresholds were unaltered in saline-treated rats, nicotine reduced reward thresholds. An injection of lorcaserin (0.3 mg/kg) prior to nicotine prevented the reward-enhancing effect of nicotine across multiple test sessions. These results demonstrated that lorcaserin reduces the rewarding value of BSR and also prevents nicotine from facilitating ICSS. Hence, lorcaserin may be effective in treating psychiatric disorders, including obesity and nicotine addiction, by reducing the value of food or drug rewards.

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Section: Results and Discussionsupporting

confidence: 89%

Section: ■ Results and Discussionsupporting

confidence: 71%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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The Serotonin 2C Receptor Agonist Lorcaserin Attenuates Intracranial Self-Stimulation and Blocks the Reward-Enhancing Effects of Nicotine

Zeeb

Higgins

Fletcher

2015

ACS Chem. Neurosci.

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“…75 Both SCH 23390 and the potent and selective 5-HT2C agonist CP 809,101 inhibit ICSS (aversive) in rats. 58 Pretreatment with the 5-HT2C antagonist SB 242084 blocks the effects of CP 809,101 but not the effects of SCH 23390 on ICSS responding. This suggests that the aversive effects of SCH 23390 are not mediated via 5-HT2C receptors.…”

Section: Discussionmentioning

confidence: 98%

Dopamine D1‐like receptor activation decreases nicotine intake in rats with short or long access to nicotine

et al. 2023

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The use of nicotine and tobacco products is highly addictive. The dopaminergic system plays a key role in the initiation and maintenance of nicotine intake. Dopamine D1‐like receptor blockade diminishes nicotine intake in rats with daily short (1 h) access to nicotine, but little is known about the effects of dopamine receptor antagonists or agonists on nicotine intake in rats with intermittent long (23 h) access. Because of the extended access conditions and high nicotine intake, the intermittent long access procedure might model smoking and vaping better than short access models. We investigated the effects of the dopamine D1‐like receptor antagonist SCH 23390 and the D1‐like receptor agonist A77636 on nicotine intake in male rats with intermittent short or long access to nicotine. The rats self‐administered nicotine for 5 days (1 h/day) and were then given 15 intermittent short (1 h/day) or long (23 h/day) access sessions (3 sessions/week, 0.06 mg/kg/inf). The D1‐like receptor antagonist SCH 23390 decreased nicotine intake to a similar degree in rats with short or long access to nicotine. The D1‐like receptor agonist A77636 induced a greater decrease in nicotine intake in the rats with long access to nicotine than in rats with short access. Treatment with A77636 induced a prolonged decrease in nicotine intake that lasted throughout the dark and light phase in the long access rats. These findings indicate that blockade and stimulation of D1‐like receptors decrease nicotine intake in an intermittent long access animal model that closely models human smoking and vaping.

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Evaluation of chemically diverse 5-HT2C receptor agonists on behaviours motivated by food and nicotine and on side effect profiles

Higgins

Silenieks²,

Lau³

et al. 2012

Psychopharmacology

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These studies support the utility of 5-HT2C agonists as a therapeutic approach to treat nicotine dependence. Plasma exposure levels after acute lorcaserin treatment suggest that equivalent dosages could be used to evaluate these drugs in obesity and smoking cessation trials. Finally, there may be differences in the side effect profiles between lorcaserin and CP-809101, raising the possibility for tolerability differences amongst 5-HT2C agonists.

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Evidence that the reward attenuating effect of the D1-like antagonist, SCH-23390, is not mediated by its agonist action at the 5-HT2c receptors

Cited by 5 publications

References 25 publications

The Serotonin 2C Receptor Agonist Lorcaserin Attenuates Intracranial Self-Stimulation and Blocks the Reward-Enhancing Effects of Nicotine

The Serotonin 2C Receptor Agonist Lorcaserin Attenuates Intracranial Self-Stimulation and Blocks the Reward-Enhancing Effects of Nicotine

Dopamine D1‐like receptor activation decreases nicotine intake in rats with short or long access to nicotine

Evaluation of chemically diverse 5-HT2C receptor agonists on behaviours motivated by food and nicotine and on side effect profiles

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