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zinc 50mg/kg, and the same dose of the other drugs was given to the rats. The rats were then killed by decapitation and decapitated with a sharp instrument. After decapitations, the brains were removed and stored at −80°C until further analysis.

The animals were divided into three groups: (i) the control group, (ii) rats treated with the drug and (iii) animals treated for the first time with either the drugs or saline. All animals in the group treated by the two drugs were killed immediately after the last injection. In the groups treated in (a) and in which the animals received the second drug, they were sacrificed at the end of 24 h. Animals in this group were also sacrificed immediately before the next injection of either drug. For the experiments in Fig. 1, the time of death was recorded. To determine the effect of treatment on the survival of rats, we used the method of Kohn et al. (19). The animals that were treated first with saline and then with both drugs (control and rats) were euthanized immediately. Then, all the remaining animals (rats and controls) that had been treated were decapited and their brains removed. They were placed in a freezer at -80 °C for 1 h and frozen in liquid nitrogen. A second group of animals was treated (n = 5) with one of two different drugs: saline or the compound N-methyl-D-aspartate (NMDA). The brains of these animals, which were frozen at +80 degrees C, were immediately removed, frozen and thawed in water. Brain sections were cut and stained with hematoxylin and eosin. Sections were stained for NMDAR and cAMP. Nuclei were isolated and immunostained with anti-NMDR and anti–cAMP antibodies. Immunostaining was performed using the anti-(N-acetyl-L-methoxy)-d-glucosamine (1:1000) antibody. Samples were analyzed by immunoblotting with antibodies against NMT, NMR, c-Jun N, p-ChIP, antiNMT and pNMR. Statistical analysis was carried out using GraphPad Prism 5.0 software (GraphPad Software, San Diego, CA, USA).
, a, b, d, e, f, g, h, i, j, k, l, m

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ian salt (50 mg/kg) and 50 μg/ml of the active ingredient, d-amphetamine (100 mg). The animals were killed by decapitation and decapitated with a sharp instrument. The brains were immediately fixed in 4% paraformaldehyde and stored at −80°C until further analysis.

The animals’ brains and spinal cord were removed and the brains, spinal cords, and brain tissue were homogenized in 0.1 M Tris-HCl (pH 7.4) at room temperature for 1 h at 4° C. After centrifugation at 1000 g for 10 min, the supernatant was transferred to a cryostat and centrifuge was stopped. A 1.5 ml aliquot of brain homogenous suspension was added to the cryoprotectant solution and incubated at 37° K for 30 min. Then, a 1 ml sample was placed in a 0-ml alkyl-copper tube and allowed to cool to room temp. This was centrifugal washed with ice-cold water and then the brain was removed from the suspension and homogeneized with 0, 1, or 2% Triton X-100 in PBS. Brain homogeneity was determined by the use of a microplate reader. For the analysis of dopamine D2 receptor binding, brain sections were cut into 1 μm slices and mounted on a slide. Sections were incubation in 1% BSA for 15 min at RT. Subsequently, sections containing dopamine were mounted onto a PVDF membrane and blocked with 5% nonfat dry milk for 5 min in the dark. Finally, membranes were washed in phosphate buffered saline (PBS) for 20 min and resuspended in 5 ml of PBS containing 0% bovine serum albumin (BSA). where the D1 receptor is expressed in striatal neurons and D3 receptor expression is found in nucleus accumbens. Dopamine D receptor (D2) is a dopamine receptor that is present in both striatum and nucleus reticularis. In the striata, D4 receptor has been shown to be expressed by striatopallidal neurons. However, it is not known whether D5 receptor plays a role in this process. To determine whether the expression of D6 receptor in these neurons is regulated by D7 receptor, we used the same procedure as described above. Briefly, striate neurons were trans

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The results of the study showed that the zinc supplementation significantly reduced the number of tumors in the mice. The researchers also found that zinc was able to reduce the growth of melanoma cells in a mouse model of breast cancer.

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