The role of alpha-7 nicotinic receptors in food intake behaviors

McFadden, Kristina L.; Cornier, Marc‐Andre; Tregellas, Jason R.

doi:10.3389/fpsyg.2014.00553

Cited by 35 publications

(17 citation statements)

References 95 publications

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“…Conversely, knockdown of the α7 subunit in either cell type did not alter the feeding response to cytisine or nicotine. While α7 is highly expressed in the hypothalamus and may regulate other circuits controlling food intake (Jo, Wiedl, & Role, 2005;McFadden, Cornier, & Tregellas, 2014), based on these data, it appears to be unlikely that α7 regulates food intake in response to nicotine through AgRP or POMC neurons. Notably, our TRAP studies showed that α7 mRNA was enriched in other cell types in ARC compared with AgRP or POMC neurons, suggesting that signalling through this nAChR subtype occurs on as-yetunidentified cell types.…”

Section: Discussionmentioning

confidence: 99%

Molecular and cellular characterization of nicotinic acetylcholine receptor subtypes in the arcuate nucleus of the mouse hypothalamus

Calarco

Taylor

et al. 2018

Eur J of Neuroscience

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Nicotine, acting through nicotinic acetylcholine receptors (nAChRs), increases the firing rate of both orexigenic agouti-related peptide (AgRP) and anorexigenic pro-opiomelanocortin (POMC) neurons in the arcuate nucleus of the hypothalamus (ARC), yet nicotine and other nAChR agonists decrease food intake in mice. Viral-mediated knockdown of the β4 nAChR subunit in all neuronal cell types in the ARC prevents the nicotinic agonist cytisine from decreasing food intake, but it is not known whether the β4 subunit is selectively expressed in anorexigenic neurons or how other nAChR subtypes are distributed in this nucleus. Using translating ribosome affinity purification (TRAP) on ARC tissue from mice with ribosomes tagged in either AgRP or POMC cells, we examined nAChR subunit mRNA levels using real-time PCR. Both AgRP and POMC cells express a comparable panel of nAChR subunits with differences in α7 mRNA levels and a trend for difference in α4 levels, but no differences in β4 expression. Immunoprecipitation of assembled nAChRs revealed that the β4 subunit forms assembled channels with α3, β2 and α4, but not other subunits found in the ARC. Finally, using cell type-selective, virally delivered small hairpin RNAs targeting either the β4 or α7 subunit, we examined the contribution of each subunit in either AgRP or POMC cells to the behavioural response to nicotine, refining the understanding of nicotinic regulation of this feeding circuit. These experiments identify a more complex set of nAChRs expressed in ARC than in other hypothalamic regions. Thus, the ARC appears to be a particular target of nicotinic modulation.

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Section: Discussionmentioning

confidence: 99%

Molecular and cellular characterization of nicotinic acetylcholine receptor subtypes in the arcuate nucleus of the mouse hypothalamus

Calarco

Taylor

et al. 2018

Eur J of Neuroscience

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“…Following nicotine cessation, a potential target for the specific changes in carbohydrate intake seen in the present study are withdrawal-mediated decreases in serotonin. Because nAChR’s are located on serotonergic neurons and their activation increases serotonin release [94] and inhibits the production of NPY [95], removal of this inhibition following smoking cessation may lead to a compensatory increase in carbohydrate intake. Finally, orexin signaling in arcuate nucleus may be of interest, given the increase in orexin A mRNA that has been observed after NSA [96].…”

Section: Discussionmentioning

confidence: 99%

The effects of nicotine self-administration and withdrawal on concurrently available chow and sucrose intake in adult male rats

Bunney

Burroughs

Hernandez

et al. 2016

Physiology & Behavior

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Carbohydrate intake, preference, and taste thresholds may be altered in current and former cigarette smokers, which may mediate weight gain and risk for obesity in individuals who quit smoking. Attempts to model these effects in rodents have primarily used noncontingent nicotine administration. The purpose of this research was to characterize changes in chow and sucrose intake in rats during a 23-h access model of i.v. nicotine self-administration (NSA), in which rats lever-pressed for chow, sucrose, and nicotine under concurrent fixed-ratio (FR) 1 schedules. Male rats were assigned to one of three groups that differed in food and drug availability. The Nicotine C+S group had concurrent access to nicotine, chow, and sucrose. The Saline C+S group had access to saline, chow, and sucrose. The Nicotine C-Only group had access to nicotine and chow, but not sucrose. Changes in food intake and weight gain were assessed during baseline, NSA, and nicotine withdrawal (i.e., saline extinction). Weight gain was significantly slowed during NSA and increased during withdrawal, but did not differ between the nicotine groups. NSA produced a significant decrease in both chow and sucrose intake. Gradual tolerance to nicotine’s effects on sucrose, but not chow intake, occurred. During withdrawal, chow and sucrose intake increased, with a larger percent increase in sucrose intake compared to chow. The proportion of total food intake from sucrose was greater at the end of withdrawal compared to baseline, indicating a history of nicotine intake changed dietary preference. Combined, these results indicate that sucrose intake is more resistant to nicotine’s appetite suppressant effects and withdrawal from nicotine produces a greater increase in sweet food intake alongside general increases in chow intake. Changes in overall food intake in current and ex-smokers may lead to increased risk for obesity and other health problems, potentially limiting the benefit of quitting smoking.

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“…Studies have shown that nicotine, a cholinergic agonist, is capable of altering the rate of food consumption and energy expenditure, thus leading to weight changes [ 36 , 37 ]. Although the exact mechanism remains elusive, both central and peripheral mechanisms are suspected to be involved.…”

Section: Discussionmentioning

confidence: 99%

Cadmium Increases the Sensitivity of Adolescent Female Mice to Nicotine-Related Behavioral Deficits

Adeniyi

Olatunji

Ishola

et al. 2014

Behavioural Neurology

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This study investigates spatial and nonspatial working memory, anxiety related behavior, and motor activities in cadmium and/or nicotine exposed female adolescent mice. P28 female adolescent mice (albino strain) were divided into four groups of five (n = 5) mice each. A set of mice (Nic) received subcutaneous nicotine (2.0 mg/kg) while a separate set (Cd) was treated with 2.0 mg/kg cadmium (subcutaneous). For the combined treatments of cadmium and nicotine, we administered 2.0 mg/kg Nicotine and 2.0 mg/kg of Cd. Subsequently, a separate group of animals (n = 5; control) received normal saline. The total duration of treatment for all groups was 28 days (P28–P56). At P56, the treatment was discontinued, after which the animals were examined in behavioural tests. Nicotine and cadmium increased the metabolism and food intake in the female adolescent mice. This also corresponded to an increase in weight when compared with the control. However, a combined nicotine-cadmium treatment induced a decline in weight of the animals versus the control. Also, nicotine administration increased the motor function, while cadmium and nicotine-cadmium treatment caused a decline in motor activity. Both nicotine and cadmium induced a reduction in memory index; however, nicotine-cadmium treatment induced the most significant decrease in nonspatial working memory.

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The role of alpha-7 nicotinic receptors in food intake behaviors

Cited by 35 publications

References 95 publications

Molecular and cellular characterization of nicotinic acetylcholine receptor subtypes in the arcuate nucleus of the mouse hypothalamus

Molecular and cellular characterization of nicotinic acetylcholine receptor subtypes in the arcuate nucleus of the mouse hypothalamus

The effects of nicotine self-administration and withdrawal on concurrently available chow and sucrose intake in adult male rats

Cadmium Increases the Sensitivity of Adolescent Female Mice to Nicotine-Related Behavioral Deficits

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