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

Abstract

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.

Self-Administered Nicotine Suppresses Body Weight Gain Independent of Food Intake in Male Rats

“…The suppression of food intake by noncontingent nicotine delivery may be directly related to the elevation of CORT following experimenter-administered nicotine, as mentioned above. In a more recent study, however, Bunney (nèe Grebenstein) et al 35 extended these results by demonstrating that self-administration of 60 μg/kg/infusion nicotine in 23-hour sessions suppressed chow pellet intake, replicating work by O'Dell and colleagues. 36 The differences between the effects of self-administered nicotine on food intake in 1-hour limited access and 23-hour extended access sessions could be due to several reasons.…”

Self-administered nicotine differentially impacts body weight gain in obesity-prone and obesity-resistant rats

“…Self-administered nicotine in extended access 23-h sessions has been demonstrated to suppress responding for chow pellets [23,24], but not responding for sucrose [23]. Smokers experience intermittent increases in blood and brain nicotine levels, which can be modeled using 1-h or 23-h access protocols.…”

Effects of acute and chronic nicotine on catecholamine neurons of the nucleus of the solitary tract

“…It acts at nicotinic acetylcholine receptors (nAChRs), ligand-gated ion channels whose endogenous neurotransmitter is acetylcholine (ACh). In addition to modulating reward, nicotine also stimulates a stress response, modulates cardiovascular and gastric reflexes, inhibits food intake, and reduces body weight (3,12,30,34,40,49,81,92), all behaviors and reflexes influenced by neurons in the nucleus of the solitary tract (NTS) in the hindbrain (1,10,38,60,63,77,79,84,91,95). The peripheral effects of nicotine on the hypothalamic-pituitary-adrenal (HPA) axis are blocked by nAChR antagonists injected into the hindbrain (59).…”