Vitamin C supplementation promotes locomotor and exploratory behaviors in male Wistar rats exposed to varying stress models.

Constant exposure to environmental stress has negative behavioral outcomes. Considering the inverse relationship between stress and Vitamin C intake, this study was aimed at investigating variable stress techniques and Vitamin C supplementation on exploratory/locomotor behaviors in male Wistar rats. Twenty-eight male Sprague-Dawley rats (100g-120g) were allotted into four groups (n=7). Control received 10ml/kg distilled water, group two received 100 mg/kg vitamin C, group three was exposed to different models of stress while group four was stressed alongside 100 mg/kg vitamin C. Vitamin C treatments were given orally for 2 weeks. Animals in groups 3 and 4 were stressed every other day with models such as multiple cage changes, exposure to noise, overnight strange objects, overnight wetting of beddings, and immobility. Explorative and locomotor activities were assessed with the open field test, novel object recognition test, and Y maze test using a Logitech camera and ANY-maze software to track the movement of the rats. Cortisol was assayed in the serum using Enzyme-linked Immuno Assay (ELISA) kit. Superoxide Dismutase, catalase, and lipid peroxidase; malondialdehyde (MDA) were also assayed in the serum. The results show that locomotor activities such as distance traveled, average speed, and time spent in the center square was significantly reduced by stress. These activities were improved with the intake of vitamin C compared with stress. Explorative activities such as locomoting around the environment, orientating towards novelty, and touching or sniffing novel objects were significantly increased in the rats on Vitamin C supplements and reduced in the stressed group. In the serum, cortisol level was significantly increased in rats exposed to stress and decreased with Vitamin C intake. Stress also significantly increased MDA and decreased SOD and CAT while vitamin C supplement decreased MDA and increased SOD and CAT. In conclusion, oral intake of vitamin C enhanced explorative/locomotor behavior and increased oxidative stress in rats exposed to different models of stress.

Neuronal Function in Male Sprague Dawley Rats During Normal Ageing.

During normal ageing, there are physiological changes especially in high energy demanding tissues including the brain and skeletal muscles. Ageing may disrupt homeostasis and allow tissue vulnerability to disease. To establish an appropriate animal model which is readily available and will be useful to test therapeutic strategies during normal ageing, we applied behavioral approaches to study age-related changes in memory and motor function as a basis for neuronal function in ageing in male Sprague Dawley rats. 3 months, n=5; 6 months, n=5 and 18 months, n=5 male Sprague Dawley Rats were tested using the Novel Object Recognition Task (NORT) and the Elevated plus Maze (EPM) Test. Data was analyzed by ANOVA and the Newman-Keuls post hoc test. The results showed an age-related gradual decline in exploratory behavior and locomotor activity with increasing age in 3 months, 6 months and 18 months old rats, although the values were not statistically significant, but grooming activity significantly increased with increasing age. Importantly, we established a novel finding that the minimum distance from the novel object was statistically significant between 3 months and 18 months old rats and this may be an index for age-related memory impairment in the NORT. Altogether, we conclude that the male Sprague Dawley rat show age-related changes in neuronal function and may be a useful model for carrying out investigations into the mechanisms involved in normal ageing.

Melatonin modulates neuronal mitochondria function during normal ageing in mice.

Mitochondrial dysfunction has been shown to be associated with normal ageing and may account for age-related vulnerability to disease. The increasing number of old people worldwide has created the need to find effective therapeutic agents to reduce the incidence of age-related disease. In the current report, we carried out an assessment of mitochondrial function in established young, middle-aged and old synaptosomal mitochondria bearing cybrids without or with melatonin treatment. The cybrids were generated by transferring isolated mitochondria from synaptosomes of brain cortical cells in mice to rho-zero mtDNA-less cells. In galactose media, a selective media that tests a cells ability to produce ATP through the electron transport chain and oxidative phosphorylation, 500µM melatonin (N-acetyl-5-methoxytryptamine) raised cell viability in young and middle-aged cybrids (P<0.05) and a concentration of 1mM raised cell viability in the old cybrids (P<0.05). The mitochondrial membrane potential (MMP) was lowered in the young cybrids (P<0.05) treated with melatonin, but it was raised in the middle-aged and old cybrids (P<0.05) with melatonin treatment. The levels of reactive oxygen species were significantly lower in the melatonin treated middle-aged and old cybrids compared with controls (P<0.05). Furthermore, ATP measurements showed no significant increase in the young cybrids (P>0.05), but increased significantly in the middle-aged and old cybrids (P<0.05) with melatonin treatment. Light and fluorescence microscopy showed observable structural damage and cell death in the middle-aged and old cybrids without melatonin treatment. The results suggest that melatonin may be a potent therapeutic intervention during age-related neuronal mitochondrial dysfunction.