A Degu Field Notebook: Seasonality of the stress response

The natural world is dynamic, ever-changing environment. As the seasons progress, organisms experience fairly predictable changes in temperature, precipitation, and photoperiod (length of daylight). Just as the environment is not a static world, neither is an animal’s ability to cope with environmental challenges.

Research has shown that many animals display seasonal patterns in both baseline and stress-induced glucocorticoid concentrations. For the white-crowned sparrow (WCS), the highest CORT (in this case, corticosterone) levels occur during the breeding season while the lowest CORT levels are seen during molt. Previous research on degus has shown that the highest concentrations of CORT (cortisol) occur during lactation.

There are many different hypotheses for why we see these seasonal differences in the stress response, but here are the main three:

Energy mobilization hypothesis: Because CORT’s metabolic effects help increase the amount of available energy, this hypothesis predicts that high levels of CORT will occur during energetically costly periods. This is the case for both WCS and degus, as breeding (for WCS) and lactation (for degus) are very energetically costly life history stages.

The behavior hypothesis: CORT also has many functions on behavior- this hypothesis states that animals modulate their CORT levels depending on the type of behavior that the season requires. This is probably best explained by an example: If a bad storm comes through when a WCS has just laid eggs (this means it’s the beginning of the breeding season), then it makes sense for the WCS to abandon its nest and flee to safety since their reproductive effort is, at the time, rather low, and the WCS can start another clutch later. But, if a bad storm occurs when a WCS has several-day old chicks (this would be during the late breeding season), then it is probably in the best interest of the WCS to try to ride out the storm since their reproductive investment is rather high. According to this hypothesis, we would expect to see high levels of CORT during the early breeding season (since high levels of CORT are correlated with movement) and low levels of CORT during the late breeding season. As it turns out, this is exactly what we see in wild WCS. But, what is unexplained is why levels during the late breeding season are still higher than any of the non-breeding life history stages.

The preparative hypothesis: In my previous blog post I mentioned that CORT helps prime the fight-or-flight response, another essential component of the stress response. In addition to priming the fight-or-flight response, elevated baseline levels of CORT also have permissive functions on the immune, metabolic, and reproductive systems in order to help an animal get ready for a stressful period. The preparative hypothesis predicts that animals increase baseline levels of CORT during life history stages when there’s a predictably greater risk of encountering severe stressors. This hypothesis hasn’t been as well studied as the other two because determining the risk of experiencing adverse conditions is difficult to define and measure.

While the seasonality of the stress response has been relatively well studied in birds, there are fewer field studies examining the seasonal stress hormone profiles of mammals. Of these mammalian studies, few actually measure baseline glucocorticoid levels. Measuring baseline CORT is difficult because CORT starts to increase after the onset of a stressor, so most animals must be bled within 3 minutes of capture (the 3-minute rule is a pretty universal rule in field endocrinology). Trapping mammals is difficult because you often need many, many traps spread across a large area, so most researchers collect blood samples after trapping for a period of a few hours.

One of the aims of my research is to determine the seasonal stress profile of the degu. I am hoping to improve upon a previous study that measured CORT after a trapping period of 2 hours. Here are the four blood samples that I take from each animal:

Baseline: This sample is taken within 3 minutes of capture. This sample is the most important of the four because it allows me to determine what kind of CORT levels an animal is typically experiencing on a day-to-day basis.

Stress-induced: I take this blood sample 30 minutes after an animal is trapped. Capture is a major stressor (it’s basically a simulated predation event from the animal’s point-of-view), so this sample will help me determine how high an animal’s CORT levels can get after encountering a significant stressor.

DEX: After I take the stress-induced sample, I then give the animal an injection of dexamethasone (DEX). DEX is a synthetic glucocorticoid and binds to CORT receptors, thus initiating negative feedback. After waiting for 90 minutes, I then take another blood sample, which will tell me how well the animal can turn of its stress response. The ability to turn off the stress response is really important because high, continuous levels of circulating glucocorticoids can start to cause problems (this is termed chronic stress, and some of the pathologies include reproductive suppression, immunosuppression, and muscle-wasting). In fact, one of the hallmarks of a chronically stressed animal is poor negative feedback.

ACTH: After taking the DEX blood sample, I then inject that animal with adrenocorticotropic hormone (ACTH). ACTH is released from the anterior pituitary, travels through the bloodstream, and binds to receptors in the adrenal glands to cause an increase in CORT production and release. 15 minutes after injection, I take another blood sample. This sample will tell me the maximum amount of CORT an animal can produce. It will be interesting to compare this sample to the stress-induced sample to see whether animals are reaching their full adrenal output 30 minutes after capture.

The blood samples that I’m collecting are not the full story of the stress profile, though. Changes in levels of the carrier protein, corticosterone binding globulin (CBG), could affect the availability of biologically active CORT. The role of CBG is unclear, though; many biologists claim that because CBG-bound CORT is unable to bind to receptors, then high levels of CBG decrease the amount of “free CORT.” On the other hand, CORT is a steroid hormone (it’s lipid soluble, not water soluble), so in order to circulate through the bloodstream, it may be necessary to have a protein carrier in order to reach all of the target tissues.

Density and distribution of CORT receptors may also play a large role in the seasonal regulation of the vertebrate stress response. CORT can only exert its physiological effects by binding to receptors, so if changes in CORT receptors mirror that of changes in CORT concentrations, then an animal’s stress response may not be changing over the seasons. Measuring CORT receptors takes a lot of time because the receptor protocol needs to be optimized for each tissue type. I won’t be attempting this, but my lab-mate is currently doing some really cool, cutting-edge research on the seasonal regulation of CORT receptors in the house sparrow.

So far, I have collected blood samples from male and female degus during the breeding/early pregnancy and late pregnancy time points. I probably will not have time to take full stress series on the lactating females this year, but I hope to return to Chile next September to get these samples.