Nicotine administration enhances NPY expression in the rat hypothalamus

Li, Ming D.; Kane, Justin K.; Parker, Steven L.; McAllen, Kathy; Matta, Shannon G.; Sharp, Burt M.

doi:10.1016/s0006-8993(00)02283-6

Cited by 112 publications

(82 citation statements)

References 36 publications

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“…The route of administration was chosen to ensure equal amounts of nicotine or saline given in an identical manner, thereby reducing potential experimental errors in the measured gene expression levels, which were induced by variation among animals. While it does not mimic human smoking exactly, this protocol does reproduce the cyclical levels of plasma nicotine concentration observed in smokers between waking and sleeping hours [2,3,36]. By using an initiation phase for habituation and an appropriate saline-control group, we believe the stress of ip injection has been taken into account, which has been documented in the c-fos expression study [47].…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, this dose and method of administration have been utilized effectively in a number of research laboratories (e.g., see Refs. [2,3,14,36,40]). …”

Section: Discussionmentioning

confidence: 99%

“…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: 98%

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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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Section: Discussionmentioning

confidence: 99%

“…Indeed, this dose and method of administration have been utilized effectively in a number of research laboratories (e.g., see Refs. [2,3,14,36,40]). …”

Section: Discussionmentioning

confidence: 99%

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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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“…Among these is the gene coding for tyrosine hydroxylase, which is involved in a rate-limiting step in catecholamine synthesis (5,6), as well as genes involved in the regulation of food intake and energy expenditure, such as neuropeptide Y, orexins, and their receptors (7,8). In addition, nicotine, like other substances of abuse, such as cocaine and alcohol, induces the expression of immediate early genes such as c-fos and junB in various brain regions (9 -11).…”

Section: Nicotinic Acetylcholine Receptors (Nachr)mentioning

confidence: 99%

Nicotine Modulates the Expression of a Diverse Set of Genes in the Neuronal SH-SY5Y Cell Line

Dunckley

Lukas

2003

Journal of Biological Chemistry

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“…For example, acute single injection of nicotine was reported to increase mRNA levels of tyrosine hydroxylase, a rate-limiting step in catecholamine synthesis, in NAs and VTA [6,49]. Chronic exposure to nicotine induced long-term increases in the mRNA expression levels of genes involved in the regulation of food intake and energy expenditure, such as neuropeptide Y (NPY), orexins, and their receptors [27,22]. Similar to other addictive substances, such as cocaine and alcohol, nicotine also was shown to induce immediate early gene expression, e.g.…”

Section: Introductionmentioning

confidence: 99%

Region-specific transcriptional response to chronic nicotine in rat brain

et al. 2001

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Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs were used to assess the transcriptional response to chronic nicotine treatment in rat, based on four brain regions, i.e. prefrontal cortex (PFC), nucleus accumbens (NAs), ventral tegmental area (VTA), and amygdala (AMYG). On the basis of a non-parametric resampling method, an index (called jackknifed reliability index, JRI) was proposed, and employed to determine the inherent measurement error across multiple arrays used in this study. Upon removal of the outliers, the mean correlation coefficient between duplicate measurements increased to 0.978±0.0035 from 0.941 ±0.045. Results from principal component analysis and pairwise correlations suggested that brain regions studied were highly similar in terms of their absolute expression levels, but exhibited divergent transcriptional responses to chronic nicotine administration. For example, PFC and NAs were significantly more similar to each other (r=0.7; P<10 −14 ) than to either VTA or AMYG. Furthermore, we confirmed our microarray results for two representative genes, i.e. the weak inward rectifier K + channel (TWIK-1), and phosphate and tensin homolog (PTEN) by using real-time quantitative RT-PCR technique. Finally, a number of genes, involved in MAPK, phosphatidylinositol, and EGFR signaling pathways, were identified and proposed as possible targets in response to nicotine administration.

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Nicotine administration enhances NPY expression in the rat hypothalamus

Cited by 112 publications

References 36 publications

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

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

Nicotine Modulates the Expression of a Diverse Set of Genes in the Neuronal SH-SY5Y Cell Line

Region-specific transcriptional response to chronic nicotine in rat brain

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