Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2012 Feb 16;8(2):e1002379. doi: 10.1371/journal.pcbi.1002379

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Sriram et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

PMC Copyright notice

Sensitivity analysis shows that the sensitivity of cortisol with respect to K for depressed subjects is much higher than for normal subjects, while for PTSD is much lower. This difference is due to the difference in the sensitivity of the HPA axis for normal, depressed, and PTSD subjects. On the other hand, hardly any difference in the sensitivity to k is seen. No sensitivity to the Hill coefficient n is observed, which is the homodimerization of GR receptor, indicating that the circadian oscillations are due to the other Hill coefficient n, that determines the nonlinearity and robustness of the oscillations. The most sensitive parameter is the total glucocorticoid receptor, which plays a strong role in cortisol feedback regulation. This is in tandem with the hypothesis. The insensitive parameters V, K, are the enzymatic degradation of the cortisol, while K is the autonomous/dilution rate of the CRH. This indicates that in the model cortisol enzymatic degradation is not necessary, because of the strong binding rates (k highly sensitive) of the GR receptors and, the autonomous degradation k (again highly sensitive), that removes the cortisol much more efficiently than the enzymatic degradation.

Inline graphic — Sensitivity analysis shows that the sensitivity of cortisol with respect to K for depressed subjects is much higher than for normal subjects, while for PTSD is much lower. This difference is due to the difference in the sensitivity of the HPA axis for normal, depressed, and PTSD subjects. On the other hand, hardly any difference in the sensitivity to k is seen. No sensitivity to the Hill coefficient n is observed, which is the homodimerization of GR receptor, indicating that the circadian oscillations are due to the other Hill coefficient n, that determines the nonlinearity and robustness of the oscillations. The most sensitive parameter is the total glucocorticoid receptor, which plays a strong role in cortisol feedback regulation. This is in tandem with the hypothesis. The insensitive parameters V, K, are the enzymatic degradation of the cortisol, while K is the autonomous/dilution rate of the CRH. This indicates that in the model cortisol enzymatic degradation is not necessary, because of the strong binding rates (k highly sensitive) of the GR receptors and, the autonomous degradation k (again highly sensitive), that removes the cortisol much more efficiently than the enzymatic degradation.