Neuropsychopharmacology (2012) 37, 2456-2466; doi:10 1038/npp 201

Neuropsychopharmacology (2012) 37, 2456-2466; doi:10.1038/npp.2012.104; published online 27 June 2012″
“Nicotine has been reported to produce both anxiolytic and/or anxiogenic effects in humans and animals.

This study examined whether pretreatment with nicotine would alter anxiety in a unique runway model of approach-avoidance conflict.

Food-restricted rats were trained to run a straight alley once a

day to obtain food upon goal-box entry. Beginning on trial 11, food reward was followed by a series of five foot shocks (0.3-0.4 mA, 0.5 s) in the goal box. Non-shocked control rats continued to run for food only. The resulting association of the goal box with both a positive (food) and negative (foot shock) Defactinib stimulus produced an approach-avoidance conflict (subjects exhibited “”retreat behaviors”" in which they would approach the goal box, stop, and then retreat back towards the start box). Once retreats were established, their sensitivity to nicotine pretreatment (0.0, 0.03, 0.045,

0.06, or 0.075 mg/kg, i.v.) was compared to saline. In subsequent tests, the effects of nicotine (0.06 or 0.03 mg/kg) were examined on spontaneous activity (locomotion) and center-square entries in an open field (anxiety).

Doses of 0.06 and 0.075 mg/kg, but not lower doses of nicotine, reduced the number of runway retreats, selleck kinase inhibitor and 0.06 mg/kg nicotine increased the number of open-field center entries relative to saline. No effects on locomotion were observed.

Nicotine reduced approach-avoidance conflict and increased the rats’ willingness to enter the center of an open field, suggesting that the drug can produce anxiolytic properties and that such

effects may serve as an important factor in the persistence of smoking behavior.”
“Meq is the major Marek’s disease virus (MDV)-encoded oncoprotein and is essential for T-cell lymphomagenesis. Meq and several noncoding RNAs, including three microRNA (MiR) clusters, are expressed from the repeats of the MDV genome during latent infection of T cells. To investigate the state of the chromatin in this and flanking regions, we carried out chromatin immunoprecipitation (ChIP) analysis of covalent histone modifications and associated bound proteins. T-cell lines selleck chemicals and a lymphoma were compared. The chromatin around the promoters for Meq and the noncoding RNAs in both cell lines and the lymphoma were associated with H3K9 acetylation and H3K4 trimethylation, which are marks of transcriptionally active chromatin. These correlated with bound Meq-c-Jun heterodimers. The only binding site for Meq homodimers is located at the lytic origin of replication (OriLyt), next to the lytic gene pp38. This region lacked active marks and was associated with repressive histone modifications (H3K27 and H3K9 trimethylation). DNA CpG methylation was investigated using methylated DNA precipitation (MeDP).

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