Academia
Effects of Stress on the Hippocampus
According to Goleman (2006),
The hippocampus, near the amygdala in the mid-brain, is our central organ for learning. This structure enables us to convert the content of ‘working memory’—new information held briefly in the prefrontal cortex—into long-term form for storage. This neural act is the heart of learning. Once our mind connects this information with what we already know, we will be able to bring the new understanding to mind weeks or years later. (p. 273)
Everything we learn, everything we read, everything we do, everything we understand, and everything we experience count on the hippocampus to function correctly. “The continual retention of memories demands a frenzy of neuronal activity. In fact, the vast majority of neurogenesis—the brain’s production of new neurons and laying down connections to others—takes place in the hippocampus” (Goleman, 2006, p. 273). Goleman also stated, “The hippocampus is especially vulnerable to ongoing emotional distress, because of the damaging effects of cortisol” (p. 273). When the body endures ongoing stress, cortisol affects the rate at which neurons are either added or subtracted from the hippocampus. This can be a tremendous assault on learning. When the neurons are attacked by cortisol, the hippocampus loses neurons and is reduced in size. In fact, duration of stress is almost as destructive as extreme stress. Goleman explained, “Cortisol stimulates the amygdala while it impairs the hippocampus, forcing our attention onto the emotions we feel, while restricting our ability to take in new information” (pp. 273-274). He added,
The neural highway for dysphoria runs from the amygdala to the right side of the prefrontal cortex. As this circuitry activates, our thoughts fixate on what has triggered the distress. And as we become preoccupied, say, worry or resentment, our mental agility sputters. Likewise, when we are sad activity levels in the prefrontal cortex drop and we generate fewer thoughts. Extremes of anxiety and anger on the one hand and sadness on the other push brain activity beyond its zones of effectiveness. (p. 268)
While explaining the stress system, Lupien, McEwen, Gunnar, and Heim (2009) discussed the important role of the amygdala. “By contrast, the amygdala, which is involved in fear processing, activates the HPA axis in order to set in motion the stress response that is necessary to deal with the challenge” (p. 435). The other important systems that are affected by stress include inflammatory cytokines, metabolic hormones and the autonomic nervous system. The researchers also stated, “All of these are affected by HPA activity, in turn, affect HPA function, and they are also implicated in the pathophysiological changes that occur in response to chronic stress, from early experiences into adult life” (p. 435). Thus, there is a relationship between glucocorticoid level and hippocampal atrophy.
Additionally, cumulative exposure to stress-related hormones compromises the ability of neurons to withstand neuropathological insults (Sapolsky, Krey, & McEwen, 2002). It is believed that this same cascade of hormones also has a neurotoxic effect on the prefrontal cortex (Lupien et al., 2009).
According to Goleman (2006), the amygdala overrides the prefrontal cortex when involved with the fight or flight system. The prefrontal cortex is the center for critical and rational thought while the amygdala commands our emotional reactions. According to Goleman,
When we are under stress, the HPA axis roars into action, preparing the body for crisis. Among other biological maneuvers, the amygdala commandeers the prefrontal cortex, the brain’s executive center. This shift in control to the low road favors automatic habits, as the amygdala draws on our knee-jerk responses to save us. The thinking brain gets sidelined for the duration; the high road moves too slowly. (p. 268)
Thus, Goleman (2006) stated that our instinct for protection and defense moves our thinking into reactivity and away from a slower, more thoughtful, and critical approach. “As our brain hands decision making to the low road, we lose our ability to think at our best” (p. 268). Increased stress and anxiety also can impair motor performance (Noteboom et al., 2001). “The ascendant amygdala handicaps our abilities for learning, for holding information and working memory, for reacting flexibly and creatively, for focusing attention at will, and for planning and organizing effectively. We plunge into what neuroscientists call ‘cognitive dysfunction’” (p. 268). Based on findings by McEwen (1998) that increased levels of cortisol caused by excessive worry and over arousal can damage the hippocampus, Soutar (n.d.) stated, “Not only does this result in loss of short-term memory function, but also depresses immune function as the hippocampus is a key switching mechanism for global immune system function” (para. 30).
Lupien et al. (2009) explained that a rise in plasma glucocorticoid in adults can negatively affect both hippocampal volume as well as memory, and both these impairments are noted in Alzheimer’s disease. Giubilei et al. (2001) found significantly higher levels of cortisol in Alzheimer’s disease patients than controls. In addition, Aisen et al. (2000) found that Alzheimer’s disease patients treated with steady, low-dose amounts of glucocorticoid showed a cognitive decline.
There appears to be windows of vulnerability to stress. Lupien et al. (2009) discussed these sensitive periods and explained them in relation to neurotoxicity and the vulnerability hypothesis. The neurotoxicity hypothesis suggests that,
Prolonged exposure to glucocorticoid reduces the ability of neurons to resist insults, increasing the rate at which they are damaged by other toxic challenges or ordinary attrition. This hypothesis implies that a reduced hippocampal size is the end product of years or decades of PTSD, depressive symptoms, or chronic stress. (p. 441)
There is also a hyposecretion of glucocorticoids in PTSD patients as well as reduced hippocampal volume. The researchers then stated, “The vulnerability hypothesis suggests that reduced hippocampal volume in adulthood is not a consequence of PTSD, depression or chronic stress, but is a pre-existing risk factor for stress-related disorders that is induced by genetics and/or early exposure to stress” (p. 441). Hence, the vulnerability hypothesis distinguishes the idea that there is a window of vulnerability for glucocorticoid hyposecretion and, therefore, explains children and adults with PTSD. It appears that exposure to trauma and stress during these windows of vulnerability actually slow down brain development in direct relationship to the length and strength of trauma.
In fact, viewing reduced hippocampal volume in adults is a strong diagnostic tool that indicates the time of the traumatic assault as well as its nature. For example, “Exposure to adversity at the time of hippocampal development could lead to hippocampus-dependent emotional disorders, which would be different from disorders arising from exposure to adversity at times of frontal cortex development” (Lupien et al., 2009, p. 441).
Maercker, Michael, Fehm, Becker, and Margraf (2004) found that “Experiencing a traumatic event in childhood [up to 12 years] is related to higher rates of major depression than is experiencing a traumatic event in adolescence [after age 13 years]” (p. 485). Additionally, Teicher, Tomoda, and Andersen (2006) indicated that early exposure to abuse and stress is associated with reduced hippocampal volume, synaptic density, and additional brain alterations.
Hence, early brain development during times of stress and trauma can both reduce hippocampal volume as well as inhibit the natural potential of the brain’s developmental course. It is interesting to note that though the hippocampus and the frontal lobe lose volume under chronic stress, the amygdala shows volume increase when exposed to chronic stress, due to a branching, treelike arrangement of dendrites known as dendritic arborizition (Lupien et al., 2009).
The junction at which two nerve cells meet, or at which dendrite meets dendrite, is called the synapse. This is a tiny gap, and the electrical activity of the brain is conducted down the axon to the synapse. A connection is made when one of a number of chemicals is released to bridge the gap at the synapse. These chemicals are called neurotransmitters and they permit electrical activity to flow across the synapse. The speed of transmission of a neurological impulse is about 100 meters a second. The transmission of brain activity then, is not electrical, but a physical/chemical reaction to an original electrical impulse. (Rose, 1985, p. 7)
It is during childhood and adolescence that the brain both overproduces and weeds out synapses. According to Nauert (2008), “Learning and memory take place at synapses, which are junctions through which brain cells communicate. These synapses reside on specialized branchlike protrusions on neurons called dendritic spines” (para. 6).
Since the amygdala is the part of the brain that develops the slowest and increases in volume when exposed to trauma and stress, adversity can cause it to modify the direction of natural brain development. The effects of such modification might not be apparent for years until the brain’s synaptic organization is complete.
This acute effect of adversity on brain organization could have negative long-term consequences. Stress at key periods of synaptic organization could modify the trajectories of connections, leading to an incubation period, such that the effects of stress would not be apparent at the time of adversity but would emerge later, when the synaptic organization has been completed. Studies showing protracted effects of early-life stress that emerge at puberty support this suggestion. (Lupien et al., 2009, p. 441)
