Modulation of Sphingosine 1-Phosphate and Tyrosine Hydroxylase in the Stress-Induced Anxiety |
| |
Authors: | Soyong Jang Donghyun Kim Yeonju Lee Sohyeon Moon Seikwan Oh |
| |
Institution: | (1) Department of Neuroscience and Medical Research Institute, School of Medicine, Ewha Womans University, Mok-dong, Yangchon-ku, Seoul, 158-710, Korea; |
| |
Abstract: | Stress causes endocrinological changes and leads to induce anxiety. It was determined the anxiety and stress-related endocrinological
changes through the observation of the level of glucocorticoid and sphingolipid metabolites in serum after stress. Immobilized
stress and electric shock was applied to rats for 7 days. This study investigated the induction of anxiety, changes of TH
and pERK expression in cortex and amygdala after stress. Also it was determined the changes of glucocorticoid and anxiety
when the rats were given stress after amygdala lesion. The stress-given rats spent a lesser percentage of time significantly
in the open arm than the control rats. The elevated level of glucocorticoid after stress was suppressed in amygdala lesion
group. The expression of TH in the amygdala was decreased, but the expression of TH was not changed in the cortex after stress.
To investigate the changes in sphingolipid metabolites after stress, the levels of sphingosine and the phosphate form of sphingolipid
(So-1-P) were analyzed in serum. The level of So-1-P was elevated after stress and anxiety was observed after the So-1-P infusion
(100 pmol/10 μl/h, i.c.v., for 7 days). Continuous infusion of So-1-P for 7 days led to the significant decrease of TH expression
in the amygdala. In conclusion, the results of this study indicate that the lesion of amygdala suppressed the stress-induced
anxiety and elevation of glucocorticoid in serum. It was also observed that expression of TH in amygdala as well as increased
levels of glucocorticoid in serum might be responsible biomarker, at least in part, of chronic stress. These results suggest
that the elevation of So-1-P might be involved in induction of anxiety during stress by the modulation of dopaminergic system
in amygdala. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|