Edwin Glueck1, Darren Ginder1, Jeff Hyde1, Katherine North1, Jeffrey W Grimm2. 1. Department of Psychology and Program in Behavioral Neuroscience, Western Washington University, 516 High Street, Bellingham, WA, 98225-9172, USA. 2. Department of Psychology and Program in Behavioral Neuroscience, Western Washington University, 516 High Street, Bellingham, WA, 98225-9172, USA. jeff.grimm@wwu.edu.
Abstract
RATIONALE: Acute or chronic environmental enrichment (EE) reduces sucrose cue reactivity in rats. This effect may be mediated by dopamine receptors. OBJECTIVES: We examined whether dopamine D1 or D2 receptor agonism could reverse the EE effect. We also examined whether any reversal effects would vary with the incubation of sucrose craving. METHODS: Following 10 days (2 h/day) of sucrose self-administration, rats experienced either 1 or 30 days of forced abstinence and either overnight (acute) or 29 day (chronic) EE. D1 (SKF 81297; 0, 0.3, or 1 mg/kg) or D2 (quinpirole; 0, 0.1, or 0.3 mg/kg) agonist was administered systemically immediately prior to a subsequent 2-h cue reactivity test the next day (n = 9-12 per group). RESULTS: Dose-dependent effects were limited to the day 1 test. High doses of the agonists increased day 1 acute EE cue reactivity to levels comparable to control animals. On the day 30 test, SKF 81297 increased cue reactivity in acute EE, chronic EE, and control rats. In contrast, quinpirole resulted in similar cue reactivity for control and enriched rats, more from a reduction in responding by controls vs. a recovery of responding by EE-experienced rats. CONCLUSIONS: Both D1 and D2 receptors may be involved in the acute EE-mediated decrease in cue reactivity observed following 1 day of forced abstinence. In contrast, at 30 days of forced abstinence, D1 receptors may be critical in cue reactivity as SKF 81297 was effective at both restoring responding of enriched animals and potentiating responding of controls.
RATIONALE: Acute or chronic environmental enrichment (EE) reduces sucrose cue reactivity in rats. This effect may be mediated by dopamine receptors. OBJECTIVES: We examined whether dopamine D1 or D2 receptor agonism could reverse the EE effect. We also examined whether any reversal effects would vary with the incubation of sucrose craving. METHODS: Following 10 days (2 h/day) of sucrose self-administration, rats experienced either 1 or 30 days of forced abstinence and either overnight (acute) or 29 day (chronic) EE. D1 (SKF 81297; 0, 0.3, or 1 mg/kg) or D2 (quinpirole; 0, 0.1, or 0.3 mg/kg) agonist was administered systemically immediately prior to a subsequent 2-h cue reactivity test the next day (n = 9-12 per group). RESULTS: Dose-dependent effects were limited to the day 1 test. High doses of the agonists increased day 1 acute EE cue reactivity to levels comparable to control animals. On the day 30 test, SKF 81297 increased cue reactivity in acute EE, chronic EE, and control rats. In contrast, quinpirole resulted in similar cue reactivity for control and enriched rats, more from a reduction in responding by controls vs. a recovery of responding by EE-experienced rats. CONCLUSIONS: Both D1 and D2 receptors may be involved in the acute EE-mediated decrease in cue reactivity observed following 1 day of forced abstinence. In contrast, at 30 days of forced abstinence, D1 receptors may be critical in cue reactivity as SKF 81297 was effective at both restoring responding of enriched animals and potentiating responding of controls.
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