Research has shown that stress during the critical or sensitive period of development has great effects on neuroendocrine development and cardiovascular function and an organism's ability to respond to stress later in life. Sodium consumption has also been shown to potentiate cardiovascular dysfunction and alter the manner in which the hypothalamus and pituitary release hormones in response to stress events. Despite studies done in these areas, there has been no significant research done to examine the effects of chronic stress during prepubertal and prenatal developmental period in order to determine the long-term effects of stress on future neuroendocrine dysfunction nor has there been an attempt to compare the ability of male versus female organisms to cope with prepubertal stress in terms of decreased endocrine function. Our hypothesis is that stress during prenatal or prepubertal """"""""critical"""""""" periods of development will alter neurologic development and neuroendocrine functions and will subsequently affect an organism's endocrine function and alter its ability to respond normally to stressors in adulthood. Our initial aim is to determine if stress, during either prepubertal growth or prenatal development, has a significant effect on neuroendocrine and endocrine parameters such as ACTH, Vasopressin, Oxytocin, Corticosterone, B-endorphin, Testosterone, and Catecholamines. We will then examine whether there is a significant gender difference in order to establish whether males or females are better able to cope with stressors during critical periods of development. Following each experimental series, we will sacrifice animals and remove sections of brain and examine them microscopically in order to determine if exposure to stress induces changes in brain tissue structure or causes tissue damage that may indicate a reason for the organism's neuroendocrine dysfunction. These experiments may help determine the role of stress as a trigger for abnormal or blunted neuroendocrine or endocrine secretions. They may also help elucidate the period of development most sensitive to external stimuli and give us an insight into why some individuals are more prone to negative stress reactions than others.
Wang, Yongmei; Rader, A J; Bahar, Ivet et al. (2004) Global ribosome motions revealed with elastic network model. J Struct Biol 147:302-14 |
Adebodun, F; Scott, C E; Cunningham, C et al. (2000) Elevated levels of Ca(II) modulate the activity and inhibition of serine proteases: implication in the mechanism of apoptosis. Cell Biochem Funct 18:59-66 |
Scott, C E; Adebodun, F (1999) 13C-NMR investigation of protein synthesis during apoptosis in human leukemic cell lines. J Cell Physiol 181:147-52 |
Adebodun, F (1999) Phospholipid metabolism and resistance to glucocorticoid-induced apoptosis in a human leukemic cell line: a 31P-NMR study using a phosphonium analog of choline. Cancer Lett 140:189-94 |
Jordan, L M; Russo-Marie, F (1992) Purification and partial characterization of phospholipase A2 isoforms from human placenta. J Chromatogr 597:299-308 |