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Emre Yildirim Lecturer in Operational Research VideoEmre Yıldırım - Trenler (Fikri Karayel Cover)
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Known For. Nicotine is a highly addictive drug and exerts its effect partially through causing dopamine release, thereby increasing intrasynaptic dopamine levels in the brain reward systems.
Dopaine D1 receptor DRD1 mRNAs and receptors are Dopaine D1 receptor DRD1 mRNAs and receptors are localized in reward-related brain regions, which receive cholinergic input.
The aim of this study is to evaluate whether nicotine administration affects the expression of DRD1s, and if so, whether epigenetic mechanisms, such as histone acetylation, are involved.
Twenty Male Sprague Dawley rats received nicotine 0. Homogenates were divided into two parts for total RNA isolation and histone H4 acetylation studies.
DRD1 mRNA expression was significantly higher in the PFC of the nicotine-treated group compared with controls; similar trends were observed in the VTA and STR.
To study epigenetic regulation, the 2kb upstream region of the DRD1 gene promoter was investigated for histone H4 acetylation in PFC samples.
Our results suggest that intermittent subcutaneous nicotine administration increases the expression of DRD1 mRNA in the PFC of rats, and this increase may be due to changes in histone H4 acetylation of the 2kb promoter of the DRD1 gene.
The duration of nicotine withdrawal-associated deficits in contextual fear conditioning parallels changes in hippocampal high affinity nicotinic acetylcholine receptor upregulation.
A predominant symptom of nicotine withdrawal is cognitive deficits, yet understanding of the neural basis for these deficits is limited.
Withdrawal from chronic nicotine disrupts contextual learning in mice and this deficit is mediated by Withdrawal from chronic nicotine disrupts contextual learning in mice and this deficit is mediated by direct effects of nicotine in the hippocampus.
Chronic nicotine treatment upregulates nicotinic acetylcholine receptors nAChR ; however, it is unknown whether upregulation is related to the observed withdrawal-induced cognitive deficits.
If a relationship between altered learning and nAChR levels exists, changes in nAChR levels after cessation of nicotine treatment should match the duration of learning deficits.
To test this hypothesis, mice were chronically administered 6. Chronic nicotine had no behavioral effect but withdrawal produced deficits in contextual fear conditioning that lasted 4 days.
Nicotine withdrawal did not disrupt cued fear conditioning. Chronic nicotine upregulated hippocampal cytisine-sensitive nAChR binding; upregulation continued after cessation of nicotine administration and the duration of upregulation during withdrawal paralleled the duration of behavioral changes.
Changes in binding in cortex and cerebellum did not match behavioral changes. Thus, nicotine withdrawal-related deficits in contextual learning are time-limited changes that are associated with temporal changes in upregulation of high-affinity nAChR binding.
All rights reserved. PMID: [PubMed - as supplied by publisher]. Department of Psychology, Neuroscience Program, Temple University, Weiss Hall, 6th Floor, Philadelphia, PA , USA.
Valproate administration to mice increases histone acetylation and 5-lipoxygenase content in the hippocampus more. Gene expression can be regulated by chromatin remodeling induced by the opposing actions of histone acetyltransferases and histone deacetylases HDAC.
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Emre Yildirim is an editor and actor, known for Rastgele , Tatli Seyler and Kara Yazi Quick Links Biography Awards Photo Gallery.
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The Rise of Daniel Kaluuya.Interests Log in now to view their full profile. Anna Klein. Aziz Saidi.