Hypoinsulinemia may mediate the lowering of self-stimulation thresholds by food restriction and streptozotocin-induced diabetes

Carr, Kenneth D.; Kim, Gye-Young; Vaca, Soledad Cabeza de

doi:10.1016/s0006-8993(00)02143-0

Cited by 48 publications

(42 citation statements)

References 55 publications

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“…sustain the behavior (7). Collectively, these findings support the hypothesis that insulin can blunt brain reward activity, including the rewarding attributes of food.…”

supporting

confidence: 73%

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats

Figlewicz

Bennett

Aliakbari³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Figlewicz DP, Bennett JL, Aliakbari S, Zavosh A, Sipols AJ. Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats. Am J Physiol Regul Integr Comp Physiol 295: R388 -R394, 2008. First published June 4, 2008 doi:10.1152/ajpregu.90334.2008.-Findings from our laboratory and others have demonstrated that the hormone insulin has chronic effects within the CNS to regulate energy homeostasis and to decrease brain reward function. In this study, we compared the acute action of insulin to decrease intake of a palatable food in two different behavioral tasks-progressive ratios sucrose self-administration and mu opioidstimulated sucrose feeding-when administered into several insulinreceptive sites of the CNS. We tested insulin efficacy within the medial hypothalamic arcuate (ARC) and paraventricular (PVN) nuclei, the nucleus accumbens, and the ventral tegmental area. Administration of insulin at a dose that has no chronic effect on body weight (5 mU) into the ARC significantly suppressed sucrose self-administration (75 Ϯ 5% of paired control). However, although the mu opioid DAMGO, [D-Ala2,N-MePhe4,Gly5-ol]-enkephalin acetate salt, stimulated sucrose intake at all four CNS sites, the ventral tegmental area was the only sensitive site for a direct effect of insulin to antagonize acute (60 min) mu opioid-stimulated sucrose feeding: sucrose intake was 53 Ϯ 8% of DAMGO-induced feeding, when insulin was coadministered with DAMGO. These findings demonstrate that free feeding of sucrose, and motivated work for sucrose, can be modulated within unique sites of the CNS reward circuitry. Further, they support the interpretation that adiposity signals, such as insulin, can decrease different aspects of ingestion of a palatable food, such as sucrose, in an anatomically specific manner. food reward; ventral tegmental area; arcuate nucleus WE HAVE PREVIOUSLY REPORTED that insulin can act within the central nervous system (CNS) to decrease food reward, in addition to providing an energy regulatory signal at the medial hypothalamus (3,11,14,31). Intraventricular (IVT) insulin administration prevents the expression of a place preference conditioned to a high-fat food treat (11), decreases initial lick rates for preferred sucrose solutions in a lickometer task (42), and decreases sucrose self-administration (13) in rats that are not food deprived. Further, IVT insulin decreases performance in the lateral hypothalamic self-stimulation task, such that there is an increase in the electrical frequency threshold required to sustain the behavior (7). Collectively, these findings support the hypothesis that insulin can blunt brain reward activity, including the rewarding attributes of food. However, the specific CNS sites that mediate the actions of insulin in different behavioral paradigms evaluating food reward have not been determined.Both the caloric and the motivating aspects of a palatable food such as sucrose might contribute to its ingestion, or overingestion, and the CNS circuitries i...

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“…sustain the behavior (7). Collectively, these findings support the hypothesis that insulin can blunt brain reward activity, including the rewarding attributes of food.…”

supporting

confidence: 73%

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats

Figlewicz

Bennett

Aliakbari³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

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“…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). Both insulin and leptin administered intracerebroventricularly (ICV) can reverse the shifted threshold of lateral hypothalamic selfstimulation following food restriction (22,23). ICV leptin also reverses food-restrictionenhanced relapse to heroin self-administration (5).…”

Section: Introductionmentioning

confidence: 99%

Modulation of food reward by adiposity signals

Figlewicz

Naleid

Sipols

2007

Physiology & Behavior

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: Modulation Of Bsr By Leptin and Insulinmentioning

confidence: 99%

“…8,9 They have also shown that centrally administered insulin decreases the rewarding impact of PFH stimulation, increasing the frequency threshold for PFH self-stimulation. 9 It has not yet been established whether these effects are specific to restriction-sensitive sites. Given the results that we have obtained with leptin administration, it is tempting to speculate that the modulation of BSR by insulin will also depend on the sensitivity of the rewarding effects to food restriction.…”

Section: Modulation Of Bsr By Leptin and Insulinmentioning

confidence: 99%

Brain reward circuitry and the regulation of energy balance

2001

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Reward signals contribute to the regulation of energy balance by influencing switching between feeding and competing behaviors. Properties of natural rewards are mimicked by electrical stimulation of certain brain regions. The rewarding effect produced by stimulating the perifornical region of the hypothalamus is modulated by body weight and is attenuated both by leptin and insulin. Research is reviewed concerning the dependence of the rewarding effect of perifornical stimulation on longterm energy stores and the effects of two neuropeptides implicated in the regulation of energy balance, neuropeptide Y and corticotropin-releasing hormone. It is proposed that the potentiating effect of weight loss on perifornical self-stimulation is not tied to an increased propensity to eat or to an enhancement of food reward per se, but resembles the influence of long-term energy stores on non-ingestive behaviors that defend body weight, such as hoarding. International Journal of Obesity (2001) 25, Suppl 5, S17 -S21 Keywords: brain stimulation reward; lateral hypothalamus; perifornical region; leptin; insulin The role of reward in the regulation of energy balanceBehavior is both the sole source of energy input and a major channel for energy expenditure. Thus, the maintenance of energy balance depends critically on the allocation of behavior between feeding and competing activities on the one hand and between energetically expensive activities and sedentary ones on the other.Rewards, such as a food object encountered while hungry, play a fundamental role in behavioral allocation. In real time, rewarding stimuli and activities create behavioral dispositions that bias an animal to resist interruption of ongoing actions. Information about rewards, such as their intensity, kind, amount and spatiotemporal distribution, is stored in memory and is used in concert with information gleaned from current stimuli to influence switching between competing behaviors. 1 Thus, unraveling the neural circuitry that confers rewarding properties on stimuli has implications for understanding the regulation of energy balance. Brain stimulation rewardProperties of rewarding natural stimuli can be mimicked by electrical stimulation of certain brain sites. The resulting neural activation gives rise to a powerful disposition to reinitiate the stimulation and to resist breaking contact with the manipulandum that triggers the stimulator. The effect responsible for this disposition is called 'brain stimulation reward' (BSR). Information about the strength of the rewarding effect and its rate of availability are stored in memory. At least in the case of lateral hypothalamic (LH) stimulation, the rewarding effect can compete with, summate with, and substitute for the rewarding effect of natural stimuli such as food. 1 It has long been suspected that the neural system responsible for BSR is not uniform and is subdivided along functional lines. 2 In this view, the rewarding effect of stimulating some sites is related to energy balance, whereas at other sites BS...

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Hypoinsulinemia may mediate the lowering of self-stimulation thresholds by food restriction and streptozotocin-induced diabetes

Cited by 48 publications

References 55 publications

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats

Insulin acts at different CNS sites to decrease acute sucrose intake and sucrose self-administration in rats

Modulation of food reward by adiposity signals

Brain reward circuitry and the regulation of energy balance

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