Chronic ritalin administration during adulthood increases serotonin pool in rat medial frontal cortex

Ritalin has high tendency to be abused. It has been the main indication to control attention deficit hyperactivity disorder. The college students may seek for it to improve their memory, decrease the need for sleep [especially during exams], which at least partially, can be related to serotonergic system. Therefore, it seems worthy to evaluate the effect of Ritalin intake on mature brain. There are many studies on Ritalin effect on developing brain, but only few studies on adults are available. This study was undertaken to find Ritalin effect on serotonin transporter [SERT] density in medial frontal cortex [MFC] of mature rat. Thirty male Wistar rats were used in the study. Rats were assigned into five groups [n = 6 per group]: one control, two Ritalin and two vehicle groups. Twelve rats received Ritalin [20 mg/kg/twice a day] orally for eleven continuous days. After one week of withdrawal and another two weeks of rest, in order to evaluate short-term effects of Ritalin, six rats were sacrificed. Another six rats were studied to detect the long-term effects of Ritalin; therefore, they were sacrificed 12 weeks after the previous group. The immunohistochemistry was performed to evaluate the results. Immunohistochemistry studies showed a higher density of SERT in both 2 and 12 weeks after withdrawal from Ritalin intake in MFC of rat and there was no significant difference between these two groups. Our findings demonstrated both short- and long-term effects of Ritalin on frontal serotonergic system after withdrawal period

Effects of dalteparin on structure of hippocampal neurons of rats in chronic stress

Stress is defined as any environmental change that disturbs the maintenance of brain homeostasis. Stress leads to production of pro-inflammatory cytokines that provoke neurodegenerative disorders. In the present study, we investigated the effects of dalteparin on hippocampal neuronal death induced by chronic stress in rats. The study was carried out on 60 adult male wistar rats, weighing 200- 250 gr. The rats were randomly divided into three groups: control, stress and stress + dalteparin [SD] groups. Animals in the stress and stress + dalteparin group were exposed to chronic stress for 4 weeks. Animals in the stress + dalteparin [SD] group received dalteparin [70,100 and 140 IU/kg/days i.p.] during the stress period. After the last stressor animals were sacrificed and concentration of IL-6 in serum was measured using ELISA. All animals were reperfused and their brains were processed for histological analysis through Nissl analysis. We found that the serum concentration of IL-6 was significantly higher in the CMS [Chronic Mild Stress] exposure group than in the control group [p<0.05]. Moreover, dalteparin, dose dependently decreased IL-6 concentration in the SD groups. Chronic stress also resulted in significant cell loss in hippocampal CA1, CA3 and hilus. Dalteparin markedly inhibited the decreases in number of hippocamoal CA1 and CA3 [p<0.01] and hilus [p<0.05] neurons caused by chronic stress. Chronic stress damages hippocampal CA1, CA3 and hilus neurons, and dalteparin protects hippocampus from damage induced by chronic stress