Nicotine's attenuation of body weight involves the perifornical hypothalamus

Kramer, Phillip R.; Guan, Guoqiang; Wellman, Paul J.; Bellinger, Larry L.

doi:10.1016/j.lfs.2007.06.010

Cited by 12 publications

(6 citation statements)

References 63 publications

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“…More specifically, the response to milk shake minus tasteless solution was greater in smokers than in nonsmokers. These results were consistent with work that indicated a critical role for hypothalamic circuits in food reward and weight gain (17,68). Nicotine binds to specific cholinergic receptors on proopiomelanocortin neurons of the arcuate nucleus, which then project to the paraventricular nucleus where they activate the melanocortin-4 receptors that are critical for food intake and energy expenditure.…”

Section: Discussionsupporting

confidence: 90%

“…Animal studies have shown that self-administered nicotine and the direct injection of nicotine into the hypothalamus decreases food intake and leads to weight loss (17)(18)(19), possibly by modulating proopiomelanocortin neurons (20). These findings suggest that one way in which nicotine influences intake is by influencing circuits in the hypothalamus that control eating behavior.…”

Section: Introductionmentioning

confidence: 99%

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Altered hypothalamic response to food in smokers

Geha¹,

Aschenbrenner²,

Felsted³

et al. 2013

The American Journal of Clinical Nutrition

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Background: Smoking cessation is often followed by weight gain. Eating behaviors and weight change have been linked to the brain response to food, but it is unknown whether smoking influences this response. Objective: We determined the influence of smoking status (smokers compared with nonsmokers) on the brain response to food in regions associated with weight changes in nonsmokers. Design: In study 1, we used functional MRI (fMRI) to identify regions of the brain associated with weight change in nonsmokers. BMI and the brain response to a milk shake, which is a palatable and energy-dense food, were measured in a group of 27 nonsmokers (5 men). Sixteen subjects (3 men) returned 1 y later for BMI reassessment. The change in BMI was regressed against the brain response to isolate regions associated with weight change. In study 2, to determine whether smokers showed altered responses in regions associated with weight change, we assessed the brain response to a milk shake in 11 smokers. The brain response to a milk shake compared with a tasteless control solution was assessed in 11 smokers (5 men) in comparison with a group of age-, sex-and body weight-matched nonsmokers selected from the pool of nonsmokers who participated in study 1. Results: The response in the midbrain, hypothalamus, thalamus, and ventral striatum was positively associated with weight change at the 1-y follow-up in 16 nonsmokers. Compared with nonsmokers, smokers had a greater response to milk shakes in the hypothalamus. Conclusion: Smokers display an altered brain response to food in the hypothalamus, which is an area associated with long-term weight change in nonsmokers.Am J Clin Nutr 2013;97:15-22.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Altered hypothalamic response to food in smokers

Geha¹,

Aschenbrenner²,

Felsted³

et al. 2013

The American Journal of Clinical Nutrition

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“…Similarly the mu-opioid receptor agonist induced increase of feeding was inhibited by a muscarinic antagonist; water intake was not affected [148]. Nicotine administration reduced food intake, but after lesioning the NE system in the perifornical hypothalamus, nicotine had no effect thus its effect on food intake is mediated by catecholaminergic neurons within or extending through this area [149]. Cholinergic influence is shown among other by feeding-induced increase in the extracellular level of acetylcholine in the medial thalamus [150].…”

Section: Components Of Food Rewardmentioning

confidence: 99%

Heterogeneity of Reward Mechanisms

Lajtha

Sershen

2009

Neurochem Res

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The finding that many drugs that have abuse potential and other natural stimuli such as food or sexual activity cause similar chemical changes in the brain, an increase in extracellular dopamine (DA) in the shell of the nucleus accumbens (NAccS), indicated some time ago that the reward mechanism is at least very similar for all stimuli and that the mechanism is relatively simple. The presently available information shows that the mechanisms involved are more complex and have multiple elements. Multiple brain regions, multiple receptors, multiple distinct neurons, multiple transmitters, multiple transporters, circuits, peptides, proteins, metabolism of transmitters, and phosphorylation, all participate in reward mechanisms. The system is variable, is changed during development, is sex-dependent, and is influenced by genetic differences. Not all of the elements participate in the reward of all stimuli. Different set of mechanisms are involved in the reward of different drugs of abuse, yet different mechanisms in the reward of natural stimuli such as food or sexual activity; thus there are different systems that distinguish different stimuli. Separate functions of the reward system such as anticipation, evaluation, consummation and identification; all contain function-specific elements. The level of the stimulus also influences the participation of the elements of the reward system, there are possible reactions to even below threshold stimuli, and excessive stimuli can change reward to aversion involving parts of the system. Learning and memory of past reward is an important integral element of reward and addictive behavior. Many of the reward elements are altered by repeated or chronic stimuli, and chronic exposure to one drug is likely to alter the response to another stimulus. To evaluate and identify the reward stimulus thus requires heterogeneity of the reward components in the brain.

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“…Tissue sections were placed on glass slides onto a freezing plate and the striatum was micropunched under a surgical microscope using 0.75mm-diameter metal core punches (Model 15072; Ted Pella, Redding, CA, USA). Tissue concentrations of dopamine were determined using HPLC (Kramer et al, 2007;Sved, 1989). Just prior to assay, the tissue samples were weighed and sonicated in perchloric acid containing dihydrobenzylamine (DHBA) (an internal standard, 100ngml -1 ; ESA, Chelmsford, MA, USA).…”

Section: Hplcmentioning

confidence: 99%

Regulation of bat echolocation pulse acoustics by striatal dopamine

Tressler

Schwartz

Wellman

et al. 2011

Journal of Experimental Biology

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) but its effects on the mammalian vocal motor pathways have not been described. MPTP has, so far, been shown to be a potent catecholaminergic neurotoxin in primates, cats, rats, mice and pigs but its efficacy and behavioral effects were found Accepted 11 July 2011 SUMMARY The ability to control the bandwidth, amplitude and duration of echolocation pulses is a crucial aspect of echolocation performance but few details are known about the neural mechanisms underlying the control of these voice parameters in any mammal. The basal ganglia (BG) are a suite of forebrain nuclei centrally involved in sensory-motor control and are characterized by their dependence on dopamine. We hypothesized that pharmacological manipulation of brain dopamine levels could reveal how BG circuits might influence the acoustic structure of bat echolocation pulses. A single intraperitoneal injection of a low dose (5mgkg -1 ) of the neurotoxin 1-methyl-4-phenylpyridine (MPTP), which selectively targets dopamine-producing cells of the substantia nigra, produced a rapid degradation in pulse acoustic structure and eliminated the bat's ability to make compensatory changes in pulse amplitude in response to background noise, i.e. the Lombard response. However, high-performance liquid chromatography (HPLC) measurements of striatal dopamine concentrations revealed that the main effect of MPTP was a fourfold increase rather than the predicted decrease in striatal dopamine levels. After first using autoradiographic methods to confirm the presence and location of D 1 -and D 2 -type dopamine receptors in the bat striatum, systemic injections of receptor subtype-specific agonists showed that MPTP's effects on pulse acoustics were mimicked by a D 2 -type dopamine receptor agonist (Quinpirole) but not by a D 1 -type dopamine receptor agonist (SKF82958). The results suggest that BG circuits have the capacity to influence echolocation pulse acoustics, particularly via D 2 -type dopamine receptor-mediated pathways, and may therefore represent an important mechanism for vocal control in bats.

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Nicotine's attenuation of body weight involves the perifornical hypothalamus

Cited by 12 publications

References 63 publications

Altered hypothalamic response to food in smokers

Altered hypothalamic response to food in smokers

Heterogeneity of Reward Mechanisms

Regulation of bat echolocation pulse acoustics by striatal dopamine

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