Article ID Journal Published Year Pages File Type
4315537 Behavioural Brain Research 2008 11 Pages PDF
Abstract

Endogenous opioids have long been implicated in mechanisms of appetite control. A significant strand in the evidence base has been the hypophagic action of broad-spectrum opioid receptor antagonists (such as naloxone) in opiate-naïve animals. However, while much has been learned about sites of action, underlying receptor mechanisms and the role of taste hedonics, surprisingly little is known about the behavioural selectivity of naloxone-induced hypophagia. As such, two experiments employed detailed video analysis to profile the behavioural effects of naloxone (Experiment 1: 1.0–5.0 mg/kg; Experiment 2: 0.01–1.0 mg/kg) in non-deprived male rats during 1 h free-feeding tests with palatable mash. Results confirmed that, at doses ≥1.0 mg/kg, naloxone consistently suppresses food consumption and feeding behaviour but, congruent with its short biological half-life, had no carryover effects on post-treatment weight gain. Crucially, the anorectic doses of naloxone did not alter the time taken to find food or to commence feeding, the time spent feeding in the initial phase of testing, or the rate at which food was consumed. Furthermore, they neither interfered with non-ingestive components of the behavioural repertoire (e.g. locomotion, rearing) nor did they disrupt the normal structure of feeding behaviour (the behavioural satiety sequence, BSS). Rather, the principal effect of naloxone was to produce a shift to the left in (i.e. accelerate) the BSS. Findings are discussed in relation to the role of (μ) opioid receptor mechanisms in taste hedonics and the likelihood of a naloxone-induced reduction in the orosensory reward that would normally accompany/follow the ingestion of palatable food.

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