Investigation of the effects of Toxoplasma gondii on behavioral and molecular mechanism in bradyzoite stage.

Toxoplasma gondii is a single-celled parasite that causes a disease called toxoplasmosis. It can reach the central nervous system, but the mechanism of T. gondii disrupting the functioning of these brain regions occurs in bradyzoite stage of parasite, causing brain damage by forming tissue cysts in brain. In our study, the effects of T. gondii on locomotor activity, anxiety, learning and memory, and norepinephrine (NE), levodopa (L-DOPA), dopamine (DA) and 3,4-D-dihydroxyphenylacetic acid (DOPAC) catecholamines in amygdala, striatum, prefrontal cortex and hippocampus regions of the brain were investigated in bradyzoite stage. Twenty male Albino mice Mus musculus, 4-5 weeks old, weighing 20-25 g, were used. T. gondii inoculated to mice intraperitonealy with 48-50-hour passages of T. gondii RH Ankara strain. For intraperitoneal inoculation of mice 5x104 tachyzoites per mouse. No inoculation was made in control group (n: 20). Locomotor activity behavior in open field test (OFT), anxious behavior in elevated plus maze (EPM), and learning behavior in novel object recognition (NOR) tests were evaluated. NE, L-DOPA, DA and DOPAC were measured by HPLC in brain tissues of amygdala, striatum, prefrontal cortex and hippocampus. A decrease was observed in the locomotor activity, anxiety and learning values of the T. gondii group compared to the control group (p < 0.05). The heighten in NE and L-DOPA levels in amygdala tissue of T. gondii group compared to control group, an elevation in NE, L-DOPA, DA and DOPAC levels in striatum tissue, and an increase in levels of NE in prefrontal cortex tissue were detected in monoamine results. In hippocampus tissue, an increase was observed in DA levels, while a decrease was observed in NE, L-DOPA and DOPAC levels. In our study, it has been shown that T. gondii in bradyzoite stage reduces locomotor activity, causes learning and memory impairment, and has anxiogenic effects.

Effects of high-intensity interval training (HIIT) on skeletal muscle atrophy, function, and myokine profile in diabetic myopathy.

PURPOSE: Diabetes is a metabolic disorder characterized by chronic hyperglycemia due to insulin deficiency and/or loss of its action. Diabetic myopathy causes functional limitations in diabetic patients. The beneficial effects of high-intensity interval training (HIIT) are widely reported. We have hypothesized that HIIT application would prevent the development of diabetic myopathy. METHODS: Male, Wistar albino rats (10 W) were randomly divided into four groups (1)Control(C), (2)Diabetes(DM), (3)Training(HIIT), and (4)Diabetes + Training(DM + HIIT). Streptozotocin(60 mg/kg) was injected for the induction of diabetes. The maximum exercise capacity(MEC) of animals was determined by an incremental load test. HIIT protocol (4 min 85-95 % MEC, 2 min 40-50 % MEC, 6 cycles, 5 days/week) was applied for 8 weeks. In the end, functional parameters, atrophy, and resistance to fatigue in soleus and EDL muscles were evaluated. IL-6, FNDC5, and myonectin levels were measured in EDL, soleus, and serum. RESULTS: We observed atrophy, fatigue sensitivity, and proinflammatory alterations (IL-6 increase) in the EDL samples due to diabetic myopathy which were not observed in the soleus samples. HIIT application prevented the aforementioned detrimental alterations. Both force-frequency response and parallelly the twitch amplitude increased significantly in the DM + HIIT group. Half relaxation time (DT50) increased in both exercising and sedentary diabetics. FNDC5 was significantly higher in the exercising animals in soleus samples. Myonectin was significantly higher in the soleus muscle only in the DM + HIIT group. CONCLUSION: Current findings show that diabetic myopathy develops earlier in glycolytic-fast-twitch fibers(EDL) than in oxidative-slow-twitch fibers(soleus). Furthermore, HIIT application prevents atrophy in skeletal muscle, increases resistance to fatigue, and has an anti-inflammatory effect. NEW FINDINGS: The current study analyzes the myokine profile and skeletal muscle function under the effect of diabetes HIIT-type exercise. We also measured maximal exercise capacity and tailored the exercise program individually according to the result. Diabetic myopathy is an important complication of diabetes yet still, it is not understood completely. Our results show that HIIT-type training would be beneficial in diabetic myopathy but further investigation is needed to understand the whole molecular mechanism.

Effects of exercise training on anxiety in diabetic rats.

Diabetes mellitus (DM) is a common health problem, which manifests itself with chronic hyperglycemia and impaired insulin action. The prevalence of anxiety disorders tends to be high in the diabetic population. Exercise has a well-known anxiolytic effect, also demonstrated on rodents, but the effect of exercise on the DM-induced anxiety is still unknown. Female, Wistar albino rats were randomly divided into four groups (n=8) (C; EX; DM; DM+EX). DM was induced by injection (i.p.; 50 mg/kg) of Streptozotocin (STZ). Rats exercised in moderate intensity on the treadmill (15m/min; 5°; 30 min) for 5 weeks. Anxiety-like behavior (ALB) was evaluated by Open field test (OFT) and Elevated Plus Maze (EPM). According to OFT, central time and central entry have increased with in EX but not in DM+EX. There was no difference between C and DM. Central latency time didn't differ among groups. Unsupported rearing increased in both EX and DM+EX. There was no significant decrease in DM. Freezing time was significantly increased in the DM group. Exercise training reduced freezing time both in diabetic and non-diabetic animals. EPM results were similar. Time spent in open arm was increased significantly in exercise groups compared to their sedentary matches, and freezing time data were also parallel to OFT. Our study revealed that diabetes had shown an anxiogenic effect, which was not severe, and it only manifested itself on some behavioral parameters. Exercise training was reduced anxiety-like behavior both in diabetic and non-diabetic rats. However, because of the nature of exercise studies, it is hard to separate the anxiolytic effect of exercise from the alteration of locomotion.