Intraventricular insulin and leptin decrease sucrose self-administration in rats

Figlewicz, Dianne P.; Bennett, Jennifer L.; Naleid, Amy M.; Davis, Charles D.; Grimm, Jeffrey W.

doi:10.1016/j.physbeh.2006.07.023

Cited by 152 publications

(136 citation statements)

References 33 publications

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“…In adults, motivated performance for sucrose is increased following the diet intervention; this is observed specifically for 'progressive ratios' self-administration, that is, when the rat presses an increasing number of times on the lever between sucrose rewards. Further, ICV insulin and leptin are ineffective at decreasing sucrose self-administration in these rats (33). This pair of observations suggests that high fat diet experience, independent of overt obesity, can modulate the rewarding or reinforcing value of palatable foods, perhaps by inducing CNS resistance to the effects of adiposity signals.…”

Section: New Directions: Modulation Of Food Reward and Reinforcement mentioning

confidence: 81%

“…Finally, we have evaluated the ability of ICV insulin or leptin to decrease self-administration of a sucrose solution (33). This task evaluates motivation to work for a rewarding substance.…”

Section: Insulin Leptin and Food Rewardmentioning

confidence: 99%

“…Self-stimulation within certain lateral hypothalamic sites induces an eating response, and selfstimulation-induced feeding is augmented with food restriction (15). Likewise, the ability of food to condition a place preference, or self-administration of food, is increased with food deprivation (16)(17)(18)(19)(20). Since peripherally-derived signals of body adiposity or energy homeostasis, i.e., the pancreatic hormone insulin and the adipose-derived hormone leptin, have been shown to act within the CNS (21), their role in mediating the effect of food restriction on motivational behaviors has been investigated (1).…”

Section: Introductionmentioning

confidence: 99%

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Modulation of food reward by adiposity signals

Figlewicz

Naleid

Sipols

2007

Physiology & Behavior

Self Cite

138

123

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Extensive historical evidence from the drug abuse literature has provided support for the concept that there is functional communication between central nervous system (CNS) circuitries which subserve reward/motivation, and the regulation of energy homeostasis. This concept is substantiated by recent studies that map anatomical pathways, or which demonstrate that hormones and neurotransmitters associated with energy homeostasis regulation can directly modulate reward and motivation behaviors. Studies from our laboratory have focused specifically on the candidate adiposity hormones, insulin and leptin, and show that these hormones can decrease performance in behavioral paradigms that assess the rewarding or motivating properties of food. Additionally we and others have provided evidence that the ventral tegmental area may be one direct target for these effects, and we are currently exploring other potential anatomical targets. Finally, we are beginning to explore the interaction between adiposity signals, chronic maintenance diet of rats, and different types of food rewards to more closely simulate the current food environments of Westernized societies including the U.S. We propose that future studies of food reward should include a more complex environment in the experimental design that takes into account abundance and variety of rewarding foods, psychological stressors, and choices of reward modalities.

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Section: New Directions: Modulation Of Food Reward and Reinforcement mentioning

confidence: 81%

Section: Insulin Leptin and Food Rewardmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Modulation of food reward by adiposity signals

Figlewicz

Naleid

Sipols

2007

Physiology & Behavior

Self Cite

138

123

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“…Consistent with this explanation, ICV leptin reduces breakpoint operant responding in a progressive ratio reinforcement schedule (Figlewicz et al, 2006), a measure used to examine the effect of a treatment on the motivation to work for food reinforcement. Another interpretation of the data that does not involve memory is that VHPC leptin administration indirectly influenced appetitive motivational drive through mechanisms involving altered anxiety levels.…”

Section: Discussionmentioning

confidence: 93%

Hippocampal Leptin Signaling Reduces Food Intake and Modulates Food-Related Memory Processing

Kanoski

Hayes

Greenwald

et al. 2011

Neuropsychopharmacol

133

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The increase in obesity prevalence highlights the need for a more comprehensive understanding of the neural systems controlling food intake; one that extends beyond food intake driven by metabolic need and considers that driven by higher-order cognitive factors. The hippocampus, a brain structure involved in learning and memory function, has recently been linked with food intake control. Here we examine whether administration of the adiposity hormone leptin to the dorsal and ventral sub-regions of the hippocampus influences food intake and memory for food. Leptin (0.1 mg) delivered bilaterally to the ventral hippocampus suppressed food intake and body weight measured 24 h after administration; a higher dose (0.4 mg) was needed to suppress intake following dorsal hippocampal delivery. Leptin administration to the ventral but not dorsal hippocampus blocked the expression of a conditioned place preference for food and increased the latency to run for food in an operant runway paradigm. Additionally, ventral but not dorsal hippocampal leptin delivery suppressed memory consolidation for the spatial location of food, whereas hippocampal leptin delivery had no effect on memory consolidation in a non-spatial appetitive response paradigm. Collectively these findings indicate that ventral hippocampal leptin signaling contributes to the inhibition of food-related memories elicited by contextual stimuli. To conclude, the results support a role for hippocampal leptin signaling in the control of food intake and food-related memory processing.

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“…In fact, i.c.v. insulin or leptin administration reduced sucrose self administration, suppressed the conditioned place preference (CPP) for sucrose pellets and reversed CPP for high-fat (HF) food (Figlewicz et al, 2003;Figlewicz et al, 2004;Figlewicz et al, 2006). Moreover, leptin administration to the VTA decreased food intake (Hommel et al, 2006;Morton et al, 2009).…”

Section: Hypothalamic Sensing Of Lcfas and Metabolic Syndromementioning

confidence: 99%