Examination of empathy-like behaviour in nicotine-preferring rat lines.

AIM: Addiction is an important global health issue, impacting also addicts environment and society. Empathy plays crucial role in establishing successful social relationships and is a fundamental component of social life. The aim of this study is to investigate how nicotine preferring (NP) strain and oral forced nicotine administration affects empathy-like behaviour in rats, with gender differences. MATERIALS AND METHODS: Sprague-Dawley NP rats (10 males/10 females) and wild-type control rats (10 males/10 females) were used. Behavioural tests were administered to all rats before and after oral forced nicotine administration. The behavioural tests were completed in the fourth week of nicotine administration. Anxiety levels that could affect empathy-like behaviour were evaluated with open field, elevated plus maze tests and with blood cortisol levels. Oxytocin receptor and arginine vasopressin (AVP) levels, which have been shown to be related to empathy-like behaviour, were examined in the prefrontal cortex and amygdala regions using the enzyme-linked immunoassay method. RESULTS: It was observed that males from the NP strain showed less empathy-like behaviour than all other groups, and nicotine administration did not cause a significant change in the results. Higher levels of locomotor activity (LA) were found in control females than in all other groups. Blood nicotine and corticosterone levels were higher in NP rats. No significant differences were found in AVP and oxytocin receptor levels in the prefrontal cortex and amygdala.Conclusions It was found that coming from an addicted strain particularly reduces empathy-like behaviour in males.

Chronic Nicotine Consumption and Withdrawal Regulate Melanocortin Receptor, CRF, and CRF Receptor mRNA Levels in the Rat Brain.

Alterations in the various neuropeptide systems in the mesocorticolimbic circuitry have been implicated in negative effects associated with drug withdrawal. The corticotropin-releasing factor (CRF) and α-melanocyte-stimulating hormone are two peptides that may be involved. This study investigated the regulatory effects of chronic nicotine exposure and withdrawal on the mRNA levels of melanocortin receptors (MC3R, MC4R), CRF, and CRF receptors (CRFR1 and CRFR2) expressed in the mesocorticolimbic system. Rats were given drinking water with nicotine or without nicotine (control group) for 12 weeks, after which they continued receiving nicotine (chronic exposure) or were withdrawn from nicotine for 24 or 48 h. The animals were decapitated following behavioral testing for withdrawal signs. Quantitative real-time PCR analysis demonstrated that nicotine exposure (with or without withdrawal) increased levels of CRF and CRFR1 mRNA in the amygdala, CRF mRNA in the medial prefrontal cortex, and CRFR1 mRNA in the septum. Nicotine withdrawal also enhanced MC3R and MC4R mRNA levels in different brain regions, while chronic nicotine exposure was associated with increased MC4R mRNA levels in the nucleus accumbens. These results suggest that chronic nicotine exposure and withdrawal regulate CRF and melanocortin signaling in the mesocorticolimbic system, possibly contributing to negative affective state and nicotine addiction.

Chronic oral nicotine administration and withdrawal regulate the expression of neuropeptide Y and its receptors in the mesocorticolimbic system.

Neuropeptide Y (NPY) and its receptors are involved in the regulation of mood, stress, and anxiety. In parallel, NPY signaling may play a vital role in the negative affective state induced by drug withdrawal. This study examined the changes in the transcript levels of NPY, Y1, Y2, and Y5 receptors in the mesocorticolimbic system during chronic nicotine exposure and withdrawal. Rats were administered with nicotine (initial dose: 25 µg/ml, maintenance dose: 50 µg/ml, free base) in drinking water for 12 weeks. Control group received only tap water. In the final week of the study, some of the nicotine-treated animals continued to receive nicotine (0-W), whereas some were withdrawn for either 24 (24-W) or 48 (48-W) h. All animals were decapitated after the evaluation of somatic signs (frequency of gasps, eye blinks, ptosis, shakes, teeth chatter) and the duration of locomotor activity and immobility. mRNA levels of NPY, Y1, Y2, and Y5 receptors in the mesocorticolimbic system were measured by quantitative real-time PCR (qRT-PCR). Results showed that nicotine withdrawal increased overall somatic signs. Moreover, chronic nicotine treatment increased the duration of locomotor activity, whereas withdrawal increased the duration of immobility. qRT-PCR analysis revealed that chronic nicotine treatment increased NPY mRNA levels in the hippocampus. On the other hand, 24- and 48-h withdrawals increased NPY mRNA levels in the amygdala and medial prefrontal cortex (mPFC), Y1 and Y2 mRNA levels in the nucleus accumbens and mPFC, and Y5 mRNA levels in the mPFC. These findings suggest that nicotine withdrawal enhances NPY signaling in the mesocorticolimbic system, which could be an important mechanism involved in regulating the negative affective state triggered during nicotine withdrawal.

The effects of extended polymerization time for different resin composites on reactive oxygen species production and cell viability.

PURPOSE: The present study was conducted to determine oxidative stress and cell viability after contact with resin composites polymerized for different times. METHODS: Disk-shaped specimens of Admira Fusion, Ceram X One Universal, Solare x and Filtek Z550 (n = 12) were prepared, and two subgroups with polymerization times of 20 and 40 s were employed. The specimens were incubated with mouse fibroblast cells for 48 and 72 h, and changes in reactive oxygen species (ROS) production and cellular viability were determined by an assay with a cell-permeable fluorescent dye, 2',7'-dichlorodihydrofluorescein diacetate (H2DCF-DA), and the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, respectively. RESULTS: At 72 h, ROS production in the presence of Admira Fusion polymerized for 40 s was reduced relative to that in the presence of Admira Fusion polymerized for 20 s (P < 0.05). Cell viability was maximal in the Admira Fusion and Solare x groups and there was no difference relative to the control group at 48 h. Cell viability was higher in the Admira Fusion and Solare x groups polymerized for 40 s than for the same materials polymerized for 20 s at 72 h (P < 0.05). CONCLUSION: Extension of the polymerizaton time has a material-specific effect and may be used as a strategy to increase the biocompability of resin composites.