Possible role of dopamine D1-like and D2-like receptors in behavioural activation and “contingent” reward evaluation in sodium-replete and sodium-depleted rats licking for NaCl solutions
ABSTRACT Based on the different effects of the dopamine D1-like and D2-like receptor antagonists SCH 23390 and raclopride on the measures of licking microstructure in rats, we suggested that the level of activation of reward-associated responses depends on dopamine D1-like receptor stimulation, and is updated, or "reboosted", on the basis of a dopamine D2-like receptor-mediated reward evaluation. To further test this hypothesis, we examined the effects of the dopamine D2-like receptor antagonist raclopride (0, 25, 125, 250μg/kg) and of the dopamine D1-like receptor antagonist SCH 23390 (0, 10, 20 and 40μg/kg) on the microstructure of licking for two different NaCl solutions (0.9% and 2.7%) in rats in sodium-replete status and in the sodium-depleted status induced by the diuretic drug furosemide. Rats were exposed to each solution for 180 seconds after the first lick. Both in sodium-replete and in sodium-depleted status, SCH 23390 produced a decrease of burst number, a measure of behavioural activation, without affecting their size, a measure of reward evaluation. Raclopride reduced burst number but appeared also to exert some effects on burst size. Sodium depletion resulted in an increased intake for both NaCl solutions due to an increase in burst number and size, and in a reduced sensitivity to the effect of raclopride on lick number. These results are not in contrast with the proposed hypothesis and are consistent with previous evidence suggesting a role for dopamine D2-like receptors in the increased NaCl appetite induced by sodium depletion.
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ABSTRACT: While the removal of the rat's olfactory bulb is considered a valid animal model of depression, recently studies found that those rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of tangles. The present study investigated the possibility of using rat's olfactory bulbectomy as a putative model for Alzheimer's disease. Olfactory bulbectomy indeed mimics a complex of Alzheimer's symptoms. We evaluated the effect of pretreatment with a specific mixture of omega-3/omega-6 fatty acids: After olfactory bulbectomy, the rats were cognitive impaired, hyperactive, anorectic, and hyperthermic and expressed increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. Pretreatment with a specific mixture of omega-3/omega-6 fatty acids blocked these adverse effects. We recommend using this model to scan potential new anti-Alzheimer's drugs and to investigate the role of fatty acids in Alzheimer's disease.
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ABSTRACT: RATIONALE: We recently suggested that dopamine on D1-like receptors is involved in the activation of goal-directed responses and the level of response activation is "reboosted" on the basis of an evaluation process involving D2-like receptors assessing "response efficacy". A main piece of evidence in support of this hypothesis was the observation of an "extinction mimicry" effect in the time course of licking bursts after dopamine D2-like receptor blockade in rats licking for sucrose. OBJECTIVES: The aim of this study was to determine whether the pattern of licking observed with sucrose as a reward could be reproduced in rats licking for a different reward (0.9 % NaCl). MATERIALS AND METHODS: We investigated the effects of the dopamine D1-like receptor antagonist SCH 23390 (0.01-0.04 mg/kg) and of the dopamine D2-like receptor antagonist raclopride (0.025-0.25 mg/kg) on the microstructure of licking for a 0.9 % NaCl solution in 12-h water-deprived rats in 30-min sessions. RESULTS: As previously observed with sucrose as a reward, raclopride reduced the size of licking bursts and produced on the burst number time course an "extinction mimicry" effect, while SCH 23390 reduced licking exclusively by reducing burst number. CONCLUSIONS: These results are consistent with the proposed hypothesis and provide support to the use of the study of licking microstructure as a valid model not only for the investigation of the mechanisms governing ingestive behaviour but also for the investigation of the mechanisms underlying behavioural activation and the related evaluation processes.Psychopharmacology 04/2013; 229(2). DOI:10.1007/s00213-013-3110-0 · 3.88 Impact Factor
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ABSTRACT: LIN, J.-Y., J. Arthurs and S. Reilly. Conditioned taste aversion: Palatability and drugs of abuse. NEUROSCI BIOBEHAV REV XX(x) XXX-XXX, 2014. - We consider conditioned taste aversion to involve a learned reduction in the palatability of a taste (and hence in amount consumed) based on the association that develops when a taste experience is followed by gastrointestinal malaise. The present article evaluates the well-established finding that drugs of abuse, at doses that are otherwise considered rewarding and self-administered, cause intake suppression. Our recent work using lick pattern analysis shows that drugs of abuse also cause a palatability downshift and, therefore, support conditioned taste aversion learning.Neuroscience & Biobehavioral Reviews 05/2014; 45. DOI:10.1016/j.neubiorev.2014.05.001 · 8.80 Impact Factor
Paolo Stefano D'Aquila