Professor Bell Lecture
Stress on the Brain: The HPA Axis and Behavior !
Margaret Bell, a researcher on Neuropsychology and Biological Psychology at the
University of Texas at Austin, came to Trinity to give a lecture titled “Stress on the Brain: The
HPA Axis and Behavior.” Since she may potentially be a professor at Trinity in upcoming years,
Ms. Bell gave this lecture in the way that she would teach a class, so students could get a taste of
her teaching style. In her lecture, she diagrammed two main points: how the HPA axis is
organized, and what negative feedback is/how it works with the HPA axis.
In order to address the HPA system, we first need to talk about the basic endocrine system
in the human body. There are two main types of hormones that act in the human body: protein
hormones and steroid hormones. Steroid hormones, made up of fatty substances such as lipids
and cholesterol, can move right through the phospholipid bilayer of a cell. Hormones that cannot
do this, such as protein hormones, must use membrane receptors in order to get inside of the cell,
and nuclear receptors to then get into the nucleus of that cell. These nuclear receptors activate
2nd messengers in the cell. The membrane receptors activate the creation of mRNA and can
change protein expression: basically, they can change gene expression. The changes that occur
from these two receptors combined cause changes in the brain and in behavior.
The HPA axis is a set of interactions, signals, and feedback systems between the
Hypothalamus, Pituitary gland, and Adrenal Cortex (hence the name HPA). The main function of
this axis controls the body’s reaction to stress, however it also influences processes such as
digestion and the immune system (functions that are influenced when the body goes through a
stress response). Each of the endocrine glands in the axis releases hormones and substances onto
the next. The hypothalamus releases Corticotropin Releasing Hormone (CRH) onto the Anterior
Pituitary, which then releases Adrenocorticotropic Hormone (ACTH) onto the Adrenal Cortex.
The Adrenal Cortex releases multiple glucocorticoid hormones (mostly cortisol) in response to
receiving the ACTH- however, these glucocorticoid hormones then act on the hypothalamus and
the pituitary in a negative feedback cycle.
A negative feedback cycle is often compared to a thermostat. A thermostat works because
it knows what it’s supposed to be at (set point), it senses the environment around it, and makes
changes to adjust to the environment. Our body works this way as well. When the Adrenal
Cortex receives ACTH from the pituitary, it starts producing cortisol. However, if it starts
receiving too much ACTH, the cortisol will start acting on both the hypothalamus and the
anterior pituitary, signaling them to stop. It does this by binding with receptors on these two
glands, which notifies them to stop producing CRH and ACTH.
Ms. Bell then had us do some problems in order to apply these theories on a real-life
study. The study concerned two different types of mother mice: High LG-ABN and Low LGABN.
High LG stands for High Licking/Grooming, meaning this mother paid a lot of attention to
her newborns and created a lot of space for them. On the other hand, Low LG means the
opposite: she didn’t pay a lot of attention to her newborns. The study was looking at how
offspring of these two different types of mothers would respond to stress. Overall, it was found
that offspring of High LG mothers responded to stress with less of a chemically-stressed
reaction, and they also returned to their baseline chemical levels quicker than Low LG offspring.