Abnormal Psychology

202 CHAPTER 6

Figure 6.1

and electroconvulsive therapy (ECT) can lower people’s cortisol levels in addition to

decreasing their depressive symptoms (Deuschle et al., 2003; Werstiuk et al., 1996).

The stress–diathesis model of depression receives support from several sources

(Nemeroff, 2008). For one, higher levels of cortisol are associated with decreases in

the size of the hippo campus, which thereby impairs the ability to form new memories

(of the sort that later can be voluntarily recalled)—which in turn may contribute to

the decreased cognitive abilities that characterize depression. And, in fact, researchers

have reported that parts of this brain structure are smaller in depressed people than

in those who are not depressed (Neumeister, Charney, & Drevets, 2005; Neumeister

et al., 2005), which suggests that stress affects the symptoms of depression in part by

altering levels of cortisol, which in turn impairs the functioning of the hippocampus.

In addition, the role of stress in setting the stage for depression receives sup-

port from studies of newborn rats that were separated from their mothers for

brief periods of time each day (Plotsky et al., 2005). In adulthood, these stressed

rats not only had more HPA axis activity and higher levels of corticotropin-releas-

ing factor (CRF) than their nonstressed counterparts, but they also had a greater

density of CRF receptors in certain brain areas. Consistent with these fi ndings,

Paxil, an antidepressant medication that targets serotonin, seems to decrease acti-

vation of the HPA axis in rats that have been deprived of their mother’s presence

(Plotsky, cited in Nemeroff, 1998). Moreover, when these rats are taken off Paxil,

the increased activation resumes.

However, the stress–diathesis model describes only part of the neurological

piece of depression. As noted earlier, dopamine also probably plays a role, and may

do so independently of effects of stress. In addition, there’s an intriguing twist to the

fi nding that HPA axis activity is related to depression: Whereas HPA axis activity

increases in typical depression, it decreases in atypical depression (Kasckow, Baker,

& Geracioti, 2001). This fi nding suggests that the two forms of depression may

arise in part from different neurological mechanisms.

Genetics

Twin studies show that when one twin of a monozygotic (identical) pair has MDD,

the other twin has a risk of also developing the disorder that is four times higher

than when the twins are dizygotic (fraternal; Bowman & Nurnberger, 1993; Kendler,

Karkowski, & Prescott, 1999). Because monozygotic twins basically share all of

their genes but dizygotic twins share only half of their genes, these results point to a

role for genetics in the etiology of this disorder. One possibility is that genes infl uence

how a person responds to stressful events (Costello et al., 2002; Kendler et al., 2005).

If a person is sensitive to stressful events, the sensitivity could lead to increased HPA

axis activation (Hasler et al., 2004), which in turn could contribute to depression.

6.1 • The HPA Axis Stress activates the hypothalamus, which releases

corticotropin-releasing factor (CRF), which in turn stimulates the pituitary gland to

release adrenocorticotropic hormone (ACTH), which then instructs the adrenal glands

to release cortisol. According to the stress–diathesis model of depression, people who

become depressed have high levels of cortisol, which lead to heightened reactivity to

stress and increased serotonin levels.

g

Stressor

Pituitary activity:

Pituitary releases

adrenocortico-

tropic hormone

(ACTH).

Adrenal glands

release cortisol.

Hypothalamic

activity:

Hypothalamus

releases

corticotropin-

releasing factor

(CRF).