Nicotine Up-Regulates Expression of Orexin and Its Receptors in Rat Brain

Kane, Justin K.

doi:10.1210/en.141.10.3623

Cited by 75 publications

(67 citation statements)

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“…Previous research found that chronic nicotine modulates several neuropeptides such as neuropeptide Y (40), galanin (41), and orexins (42) in the hypothalamus or in the mesolimbocortical dopamine regions. However, it was unclear if chronic nicotine altered these peptides in the DS.…”

Section: Table I Changed Prohormone-derived Peptides and Unchanged Knmentioning

confidence: 99%

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Petruzziello

Falasca

Andrén

et al. 2013

Molecular & Cellular Proteomics

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The chronic use of nicotine, the main psychoactive ingredient of tobacco smoking, alters diverse physiological processes and consequently generates physical dependence. To understand the impact of chronic nicotine on neuropeptides, which are potential molecules associated with dependence, we conducted qualitative and quantitative neuropeptidomics on the rat dorsal striatum, an important brain region implicated in the preoccupation/ craving phase of drug dependence. We used extensive LC-FT-MS/MS analyses for neuropeptide identification and LC-FT-MS in conjunction with stable isotope addition for relative quantification. The treatment with chronic nicotine for 3 months led to moderate changes in the levels of endogenous dorsal striatum peptides. Five enkephalin opioid peptides were up-regulated, although no change was observed for dynorphin peptides. Specially, nicotine altered levels of nine non-opioid peptides derived from precursors, including somatostatin and cerebellin, which potentially modulate neurotransmitter release and energy metabolism. This broad but selective impact on the multiple peptidergic systems suggests that apart from the opioid peptides, several other peptidergic systems are involved in the preoccupation/craving phase of drug dependence. Our finding permits future evaluation of the neurochemical circuits modulated by chronic nicotine exposure and provides a number of novel molecules that could serve as potential therapeutic targets for treating drug dependence. Molecular & Cellular

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Section: Table I Changed Prohormone-derived Peptides and Unchanged Knmentioning

confidence: 99%

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Petruzziello

Falasca

Andrén

et al. 2013

Molecular & Cellular Proteomics

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“…The rats quickly became tolerant to the dose, and no seizures were observed [24,36]. An initiation phase of 48 h was used to habituate the animals to the stress of the injection, as confirmed by reduction of c-fos expression [47].…”

Section: Animals Nicotine Administration and Brain Punchesmentioning

confidence: 99%

Nicotine coregulates multiple pathways involved in protein modification/degradation in rat brain

Kane

Konu

Jennie

et al. 2004

Molecular Brain Research

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Previously, we used cDNA microarrays to demonstrate that the phosphatidylinositol and MAP kinase signaling pathways are regulated by nicotine in different rat brain regions. In the present report, we show that, after exposure to nicotine for 14 days, ubiquitin, ubiquitinconjugating enzymes, 20S and 19S proteasomal subunits, and chaperonin-containing TCP-1 protein (CCT) complex members are upregulated in rat prefrontal cortex (PFC) while being downregulated in the medial basal hypothalamus (MBH). In particular, relative to saline controls, ubiquitins B and C were upregulated by 33% and 47% ( Pb0.01), respectively, in the PFC. The proteasome beta subunit 1 (PSMB1) and 26S ATPase 3 (PSMC3) genes were upregulated in the PFC by 95% and 119% ( Pb0.001), respectively. In addition to the protein degradation pathway of the ubiquitin-proteasome complexes, we observed in the PFC an increase in the expression of small, ubiquitin-related modifiers (SUMO) 1 and 2 by 80% and 33%, respectively ( Pb0.001), and in 3 of 6 CCT subunits by up to 150% ( Pb0.0001). To a lesser extent, a change in the opposite direction was obtained in the expression of the same gene families in the MBH. Quantitative real-time RT-PCR was used to validate the microarray results obtained with some representative genes involved in these pathways. Taken together, our results suggest that, in response to systemic nicotine administration, the ubiquitin-proteasome, SUMO, and chaperonin complexes provide an intricate control mechanism to maintain cellular homeostasis, possibly by regulating the composition and signaling of target neurons in a region-specific manner. D

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“…Many reports implicate nicotine as the appetite suppressing component of smoking (Grunberg, 1986;Blaha et al, 1998;Li et al, 2000;Zhang et al, 2001). Studies of feeding behavior reveal that smoking or nicotine administration decreases meal size, measured as the amount of food intake per meal, without substantial changes in meal number (Blaha et al, 1998;Miyata et al, 2001).…”

Section: Does Nicotine Affect Feeding Via Interactions At Peripheral mentioning

confidence: 99%

Nicotinic receptor‐mediated effects on appetite and food intake

Jo¹,

Talmage

Role³

2002

J. Neurobiol.

278

197

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ABSTRACT:It is well known, although not well understood, that smoking and eating just do not go together. Smoking is associated with decreased food intake and lower body weight. Nicotine, administered either by smoking or by smokeless routes, is considered the major appetite-suppressing component of tobacco. Perhaps the most renowned example of nicotine's influence on appetite and feeding behavior is the significant weight gain associated with smoking cessation. This article presents an overview of the literature at, or near, the interface of nicotinic receptors and appetite regulation. We first consider some of the possible sites of nicotine's action along the complex network of neural and non-neural regulators of feeding. We then present the hypothesis that the lateral hypothalamus is a particularly important locus of the anorectic effects of nicotine. Finally, we discuss the potential role of endogenous cholinergic systems in motivational feeding, focusing on cholinergic pathways in the lateral hypothalamus.

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Nicotine Up-Regulates Expression of Orexin and Its Receptors in Rat Brain

Cited by 75 publications

References 0 publications

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Chronic Nicotine Treatment Impacts the Regulation of Opioid and Non-opioid Peptides in the Rat Dorsal Striatum

Nicotine coregulates multiple pathways involved in protein modification/degradation in rat brain

Nicotinic receptor‐mediated effects on appetite and food intake

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