Stress and the Goldilocks Effect: How Much is Just Right?

Imagine you are running late for an important meeting, and you get stuck in bumper-to-bumper traffic. Or you just got into a fight with your closest friend. Or you lost your keys and are locked out of your house at night. Or you get pulled over by the police for speeding. Your heart might be pounding, you might be breathing fast and starting to sweat. All of these situations are examples of acute stress, meaning short-term threats or anxiety-provoking events that trigger the autonomic nervous system to spring into action. The body begins to produce cortisol and adrenaline, activating a “fight-or-flight” response that sends your body into survival mode (Shields et al., 2016). These corticosteroid stress hormones are released from the adrenal glands, which are tucked right on top of the kidneys. But they quickly communicate with the rest of the body upon release.

Acute stressors are typically thought of as unpleasant. Most people don’t enjoy being thrown into a nerve-wracking situation. And the autonomic processes triggered by these experiences are biologically taxing. However, Yuen et al. (2009) have shown that acute stress can actually have cognitive benefits. Particularly, their research suggests that acute stress can enhance working memory. Their study focuses on the hypothalamic-pituitary-adrenocortical (HPA) axis. This system is activated by stress and triggers the release of cortisol, which will then bind to mineralocorticoid receptors (MRs) and glucocorticoid receptors (GRs) (Yuen et al., 2009).

Under conditions of chronic, or long-term, stress, the consistent, repeated release of stress hormones can damage the body and impair spatial and contextual memory performance, as well as hinder attentional control (Yuen et al., 2009). However, moderate amounts of acute stress have been shown to facilitate associative learning, increase focus and enhance memory! Particularly if the acute stress occurs under the right conditions, namely in the context of learning.

There seems to be a Goldilocks effect at play in the relationship between glucocorticoid levels and cognitive effects; too many or too few stress hormones can diminish cognitive processes, while just the right amount of acute stress, under the right circumstances, can improve neural functioning. So what are the neural mechanisms behind this relationship? How is this all happening?

One key player in the acute stress/cognitive function system is the prefrontal cortex (PFC). This brain region plays a major role in high level processing and executive function, working memory, and learning. This is also one of the areas in the brain containing MRs and GRs, which creates a communication network between stress hormones and the PFC (Yuen et al., 2009). Another important neuronal component to acute stress and cognitive function is glutamate. This neurochemical is the most abundant neurotransmitter (chemical messenger) in the brain. Glutamate triggers excitatory neural systems, meaning it activates neurons to fire, by binding to several types of receptors in the PFC, including NMDA and AMPA receptors (Kemp & McKernan, 2002). This neurotransmission then facilitates working memory by fostering the creation of neuronal connections in the PFC (Houtepen et al., 2017).

Let’s put it all together now. Yuen et al. (2009) propose that acute stress in a learning environment, for example, a test-taking situation, will signal the body to produce more glutamate in the PFC. In turn, more NMDA and AMPA receptors are being activated. Simply stated, the PFC is more activated. And when your neurons are rapidly firing, your brain is better able to form new connections and store new memories. So, that surge of stress you might feel during a fast-paced class as you struggle to keep up might actually help you better remember what you are learning!

References

Houtepen, L.C, et al. “Acute stress effects on GABA and glutamate levels in the prefrontal cortex: A 7T 1H magnetic resonance spectroscopy study.” NeuroImage. Clinical vol. 14 195-200. 4 Jan. 2017, doi:10.1016/j.nicl.2017.01.001

Kemp, J., McKernan, R. NMDA receptor pathways as drug targets. Nat Neurosci 5, 1039–1042 (2002). https://doi.org/10.1038/nn936

Shields, Grant S., et al. “The Effects of Acute Stress on Core Executive Functions: A Meta-Analysis and Comparison with Cortisol.” Neuroscience & Biobehavioral Reviews, vol. 68, 2016, pp. 651–668., doi:10.1016/j.neubiorev.2016.06.038.

Yuen, E. Y., et al. “Acute Stress Enhances Glutamatergic Transmission in Prefrontal Cortex and Facilitates Working Memory.” Proceedings of the National Academy of Sciences, vol. 106, no. 33, 2009, pp. 14075–14079., doi:10.1073/pnas.0906791106.

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