This review is part of a special issue dedicated to
Opioid addiction, and examines the influential role of
opioid peptides,
opioid receptors and
opiate drugs in mediating food intake and
body weight control in rodents. This review postulates that
opioid mediation of food intake was an example of "positive addictive" properties that provide motivational drives to maintain
opioid-seeking behavior and that are not subject to the "negative addictive" properties associated with tolerance, dependence and withdrawal. Data demonstrate that
opiate and
opioid peptide agonists stimulate food intake through homeostatic activation of sensory, metabolic and energy-related In contrast, general, and particularly mu-selective,
opioid receptor antagonists typically block these homeostatically-driven ingestive behaviors. Intake of palatable and hedonic food stimuli is inhibited by general, and particularly mu-selective,
opioid receptor antagonists. The selectivity of specific
opioid agonists to elicit food intake was confirmed through the use of
opioid receptor antagonists and molecular knockdown (antisense) techniques incapacitating specific exons of
opioid receptor genes. Further extensive evidence demonstrated that homeostatic and hedonic ingestive situations correspondingly altered the levels and expression of
opioid peptides and
opioid receptors.
Opioid mediation of food intake was controlled by a distributed brain network intimately related to both the appetitive-consummatory sites implicated in food intake as well as sites intimately involved in reward and reinforcement. This emergent system appears to sustain the "positive addictive" properties providing motivational drives to maintain
opioid-seeking behavior.