Gene expression of pro-opiomelanocortin and melanocortin receptors is regulated in the hypothalamus and mesocorticolimbic system following nicotine administration

Tapinc, Damla E.; Ilgin, Rabia; Kaya, Egemen; Gozen, Oguz; Ugur, Müzeyyen; Koylu, Ersin O.; Kanıt, Lütfiye; Keser, Ayşegül; Balkan, Bedih

doi:10.1016/j.neulet.2016.11.049

Cited by 12 publications

(7 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results are consistent with previous studies that have identified increased expression of these genes following nicotine exposure [ 87 , 108 – 110 ], but opposite results have also been reported [ 111 , 112 ]. For example, Pomc upregulation has been observed in the arcuate nucleus of the hypothalamus after chronic nicotine treatment [ 108 , 110 ].…”

Section: Discussionsupporting

confidence: 93%

The influence of adolescent nicotine exposure on ethanol intake and brain gene expression

et al. 2018

View full text Add to dashboard Cite

Nicotine and alcohol are often co-abused. Adolescence is a vulnerable period for the initiation of both nicotine and alcohol use, which can lead to subsequent neurodevelopmental and behavioral alterations. It is possible that during this vulnerable period, use of one drug leads to neurobiological alterations that affect subsequent consumption of the other drug. The aim of the present study was to determine the effect of nicotine exposure during adolescence on ethanol intake, and the effect of these substances on brain gene expression. Forty-three adolescent female C57BL/6J mice were assigned to four groups. In the first phase of the experiment, adolescent mice (PND 36–41 days) were exposed to three bottles filled with water or nicotine (200 μg/ml) for 22 h a day and a single bottle of water 2 h a day for six days. In the second phase (PND 42–45 days), the 4-day Drinking-in-the-Dark paradigm consisting of access to 20% v/v ethanol or water for 2h or 4h (the last day) was overlaid during the time when the mice did not have nicotine available. Ethanol consumption (g/kg) and blood ethanol concentrations (BEC, mg %) were measured on the final day and whole brains including the cerebellum, were dissected for RNA sequencing. Differentially expressed genes (DEG) were detected with CuffDiff and gene networks were built using WGCNA. Prior nicotine exposure increased ethanol consumption and resulting BEC. Significant DEG and biological pathways found in the group exposed to both nicotine and ethanol included genes important in stress-related neuropeptide signaling, hypothalamic–pituitary–adrenal (HPA) axis activity, glutamate release, GABA signaling, and dopamine release. These results replicate our earlier findings that nicotine exposure during adolescence increases ethanol consumption and extends this work by examining gene expression differences which could mediate these behavioral effects.

show abstract

Section: Discussionsupporting

confidence: 93%

The influence of adolescent nicotine exposure on ethanol intake and brain gene expression

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Beta‐endorphin is another endogenous DOR ligand. In a previous study, we have shown that 0.6 mg/kg nicotine increased proopiomelanocortin (POMC) mRNA in the hypothalamic arcuate nucleus, a brain region which projects to the VTA (Tapinc et al, ). Accordingly, 0.6 mg/kg nicotine may enhance POMC‐derived beta‐endorphin release in the VTA and cause a further increase in DOR signaling.…”

Section: Discussionmentioning

confidence: 99%

“…Probes were labeled in the 5′ with 6‐carbossi‐fluorescein‐rhodamine (FAM) and in the 3′ end with Black Hole Quencher1 (BHQ1). qPCR was performed in a LightCycler 480 System using LightCycler 480 Probes Master (Roche Applied Science) according to thermocycler conditions recommended by the manufacturer for 96‐well plates as described previously (Kaya et al, ; Tapinc et al, ). The thermocycling reaction was initiated by activation of Taq DNA Polymerase by heating at 95°C for 5 min, followed by 45 cycles of 10 s at 95°C, 30 s at 60°C, and 1 s at 72°C, using the LightCycler 480 Real‐Time PCR Detection System (Roche Diagnostics GmbH, Mannheim, Germany).…”

Section: Methodsmentioning

confidence: 99%

Chronic nicotine-induced changes in gene expression of delta and kappa-opioid receptors and their endogenous ligands in the mesocorticolimbic system of the rat

Ugur

Kaya

Gozen

et al. 2017

Synapse

Self Cite

View full text Add to dashboard Cite

Delta and kappa opioid receptors (DOR and KOR, respectively) and their endogenous ligands, proenkephalin (PENK) and prodynorphin (PDYN)-derived opioid peptides are proposed as important mediators of nicotine reward. This study investigated the regulatory effect of chronic nicotine treatment on the gene expression of DOR, KOR, PENK and PDYN in the mesocorticolimbic system. Three groups of rats were injected subcutaneously with nicotine at doses of 0.2, 0.4, or 0.6 mg/kg/day for 6 days. Rats were decapitated 1 hr after the last dose on day six, as this timing coincides with increased dopamine release in the mesocorticolimbic system. mRNA levels in the ventral tegmental area (VTA), lateral hypothalamic area (LHA), amygdala (AMG), dorsal striatum (DST), nucleus accumbens, and medial prefrontal cortex were measured by quantitative real-time PCR. Our results showed that nicotine upregulated DOR mRNA in the VTA at all of the doses employed, in the AMG at the 0.4 and 0.6 mg/kg doses, and in the DST at the 0.4 mg/kg dose. Conversely, PDYN mRNA was reduced in the LHA with 0.6 mg/kg nicotine and in the AMG with 0.4 mg/kg nicotine. KOR mRNA was also decreased in the DST with 0.6 mg/kg nicotine. Nicotine did not regulate PENK mRNA in any brain region studied.

show abstract

“…POMC is post-translationally modified into adrenocorticotropic hormone (ACTH), beta-endorphin, and alpha-melanocytestimulating hormone (alpha-MSH) and other biologically active molecules (Raffin-Sanson et al 2003). Reward process may involve the regulation of POMC gene expression and the gene expression of POMC-derived peptide receptors (Tapinc et al 2017).…”

Section: Ethanol Exposure Effects On Methylation Levels and Gene Expmentioning

confidence: 99%

How alcohol drinking affects our genes: an epigenetic point of view

Ciafrè

Carito

Ferraguti

et al. 2019

Biochem. Cell Biol.

View full text Add to dashboard Cite

This work highlights recent studies in epigenetic mechanisms that play a role in alcoholism, which is a complex multifactorial disorder. There is a large body of evidence showing that alcohol can modify gene expression through epigenetic processes, namely DNA methylation and nucleosomal remodeling via histone modifications. In that regard, chronic exposure to ethanol modifies DNA and histone methylation, histone acetylation, and microRNA expression. The alcohol-mediated chromatin remodeling in the brain promotes the transition from use to abuse and addiction. Unravelling the multiplex pattern of molecular modifications induced by ethanol could support the development of new therapies for alcoholism and drug addiction targeting epigenetic processes.

show abstract

Gene expression of pro-opiomelanocortin and melanocortin receptors is regulated in the hypothalamus and mesocorticolimbic system following nicotine administration

Cited by 12 publications

References 34 publications

The influence of adolescent nicotine exposure on ethanol intake and brain gene expression

The influence of adolescent nicotine exposure on ethanol intake and brain gene expression

Chronic nicotine-induced changes in gene expression of delta and kappa-opioid receptors and their endogenous ligands in the mesocorticolimbic system of the rat

How alcohol drinking affects our genes: an epigenetic point of view

Contact Info

Product

Resources

About