ACUTE STRESS LEADS TO A LONG-TERM CHANGE IN THE ADRENAL LEVELS OF NEUROPEPTIDE Y.
Document Type
Presentation
Start Date
22-10-2010 10:45 AM
End Date
22-10-2010 12:00 PM
Description
The response to stress involves the activation of two pathways namely a hormonal (the HPA axis) and a neuronal pathway (the sympathetic nervous system). Activation of the HPA axis stimulates the adrenal cortex to release glucocorticoids (CORT). Neuronal activation depolarizes the chromaffin cells in the adrenal medulla leading to an increase in the secretion of catecholamines so altering blood pressure. In addition to the catecholamines, the chromaffin cells also synthesize neuropeptide Y (NPY). Although previous studies have shown that adrenal NPY is increased by various stressors, how this response is mediated at the level of single chromaffin cells and whether it has any physiological consequences is not clear. To address these questions, mice were briefly exposed to two different stressors: either fox urine exposure or the cold water forced swim test (FST), for 5-6 minutes. When measured 24 hrs later both stressors led to a significant increase in NPY-immunoreactivity (NPY-ir) in chromaffin cells measured either in vitro or in situ. When NPY-GFP transgenic mice, in which GFP is linked to the NPY promoter, were exposed to the FST, the level of GFP in single chromaffin cells was elevated suggesting that stress induced an increase in NPY promoter activity. To determine whether these effects were reversible we measured NPY-and tyrosine hydroxylase-ir (TH, a marker of catecholamine synthesis) in adrenal sections from control and stressed animals at various times after the FST. Stress increased the levels of NPY-ir and TH-ir in situ monitored after 24 hrs and the increase was reversed one week after the FST. Plasma levels of epinephrine were also consistently elevated 24 hrs after the FST (although this did not reach statistical significance). The FST also resulted in a co-activation of the HPA axis as shown by a significant increase in the plasma CORT levels measured 30 mins after the FST. Furthermore the plasma levels of CORT were still elevated 24 hrs after the FST indicating that stress had induced sustained changes in both the hormonal and neuronal pathways. These results indicate that a brief period of stress has a long-lasting effect on the synthetic capacity of the adrenal gland. Future work will explore whether the increase in adrenal NPY plays a significant role in mediating the response to stress.
Recommended Citation
Wang, Qian and Whim, M. D., "ACUTE STRESS LEADS TO A LONG-TERM CHANGE IN THE ADRENAL LEVELS OF NEUROPEPTIDE Y." (2010). Dr. Joseph M. Moerschbaecher, III Graduate Research Day. 23.
https://digitalscholar.lsuhsc.edu/grad_rs/2010/poster1/23
ACUTE STRESS LEADS TO A LONG-TERM CHANGE IN THE ADRENAL LEVELS OF NEUROPEPTIDE Y.
The response to stress involves the activation of two pathways namely a hormonal (the HPA axis) and a neuronal pathway (the sympathetic nervous system). Activation of the HPA axis stimulates the adrenal cortex to release glucocorticoids (CORT). Neuronal activation depolarizes the chromaffin cells in the adrenal medulla leading to an increase in the secretion of catecholamines so altering blood pressure. In addition to the catecholamines, the chromaffin cells also synthesize neuropeptide Y (NPY). Although previous studies have shown that adrenal NPY is increased by various stressors, how this response is mediated at the level of single chromaffin cells and whether it has any physiological consequences is not clear. To address these questions, mice were briefly exposed to two different stressors: either fox urine exposure or the cold water forced swim test (FST), for 5-6 minutes. When measured 24 hrs later both stressors led to a significant increase in NPY-immunoreactivity (NPY-ir) in chromaffin cells measured either in vitro or in situ. When NPY-GFP transgenic mice, in which GFP is linked to the NPY promoter, were exposed to the FST, the level of GFP in single chromaffin cells was elevated suggesting that stress induced an increase in NPY promoter activity. To determine whether these effects were reversible we measured NPY-and tyrosine hydroxylase-ir (TH, a marker of catecholamine synthesis) in adrenal sections from control and stressed animals at various times after the FST. Stress increased the levels of NPY-ir and TH-ir in situ monitored after 24 hrs and the increase was reversed one week after the FST. Plasma levels of epinephrine were also consistently elevated 24 hrs after the FST (although this did not reach statistical significance). The FST also resulted in a co-activation of the HPA axis as shown by a significant increase in the plasma CORT levels measured 30 mins after the FST. Furthermore the plasma levels of CORT were still elevated 24 hrs after the FST indicating that stress had induced sustained changes in both the hormonal and neuronal pathways. These results indicate that a brief period of stress has a long-lasting effect on the synthetic capacity of the adrenal gland. Future work will explore whether the increase in adrenal NPY plays a significant role in mediating the response to stress.