Early Life Stress Experiments

A critique of “Ehrlich, David E, and Donald G Rainnie. 'Prenatal Stress Alters The Development Of Socioemotional Behavior And Amygdala Neuron Excitability In Rats '.

The prefrontal cortex is known to develop in the later periods of the prenatal stages when relating to myelination, cell growth and synaptic density (Kolb et al. 2012). Since it has a prolonged development with the expression of glucocorticoid (GC) receptors, the prefrontal cortex may be prone to early insults (Kolb et al. 2012). This study was also concluded in rats that showcased a relationship between maternal stress during pregnancy and reductions of dendritic spine densities in the prefrontal cortex (Kolb et al.

Childhood trauma affects many brain systems. The stress response system and its cosystems pay the greatest toll when a child experiences chronic threat. Taking a closer look at the

The brain develops in such a way that it leaves itself vulnerable to these negative influences. The prenatal brain develops an overabundance of neurons, some of which are then carefully eliminated before age 4 (5). In a process similar to this, the amount of synapses between neurons is built up during early childhood and then pruned back for the next 30 years of life (5). These two processes are both disturbed by elevated levels of stress hormones (5). The two centers of the brain with the most postnatal changes, including the growth of new neurons after birth, are the hippocampus, which is part of the limbic system, and the cerebellar vermis (6). The hippocampus is in charge of creating and retrieving memories, working together with the other parts of the limbic system, such as the amygdala, which records the emotions for each memory. The vermis controls the production and release of two of the catecholamine neurotransmitters, dopamine and norepinephrine (6). Both the vermis and the limbic system have higher concentrations of receptors for the stress hormone cortisol than anywhere else in the brain (6). Due to this fact, these still-developing areas are the most vulnerable to the damage done by elevated levels of stress hormones.

Despite these concurring viewpoints, there are fundamental differences between these perspectives. The medical/disease perspective focuses on the costs of early stressful experiences, asserting that exposure to early life adversity disrupts normal development, causing dysregulations in biological systems (Ellis & Del Giudice, 2014). As outlined by Del Giudice and Ellis (2016), research from this perspective generally focuses on unfavorable health outcomes associated with early stress exposure, such as reduced performance on intelligence tests and greater prevalence of psychopathology. The evolutionary perspective, in contrast, extends the understanding of epigenetically-based developmental processes by examining the benefits of stress responsivity and its orchestration of adaptive developmental patterns. According to the ACM, organisms have calibrated their systems via environmental cues to adapt physiological and behavioral systems to their current and future environments (Del Giudice & Ellis, 2016). Therefore, despite potential impairments/costs, there should also be adaptations; for example, as discussed by Ellis & Del Giudice (2014), adolescents

The news article I have decided to focus on is called “Chronic Stress Can Damage brain Structure and Connectivity”. The author, Christopher Bergland, discusses a study that was done at Berkeley and researchers discovered that chronic stress actually causes long-term changes in the brain. Bergland (2014) makes an interesting point in the beginning of the article about how children who are exposed to chronic stress are more likely that have problems with anxiety and mood disorders. A majority of the article focuses on the “revolutionary” experiments Daniela Kaufter, a UC Berkeley associate professor, conducted. These experiments are so significant because they show that “chronic stress and elevated levels of cortisol can generate more overproduction of myelin-producing cells and fewer neurons than normal.” Bergland (2014) then discusses the “grey matter” in the brain, which is packed full of nerve cell bodies and is where the brain does higher functions. He also discusses “white matter”, which is full of axons that connect neurons and makes a network of communications between different regions of the brain. The author (2014) says that the white matter in the brain is called that because the myelin sheath that surrounds the axons is white and fatty “and speeds the flow of electrical signals between neurons and brain regions.” Kaufer’s experiments focus specifically on the hippocampus, which is responsible for memory and emotions and can shrink under periods of stress. The

Further research on rats show the effects of epigenetics on stress. A study by Weaver et al. (2004) showed that rat mothers that groomed their pups in the first week of its life affected how well it dealt with stressful stimuli in later life. The positive maternal behaviour committed changes to the glucocortocid receptor gene (GR). This gene turns off the (short term) stress response (that occurs via the pituitary-adrenal system). In early pup development this gene is silenced. With grooming it was unmethylated, unsilencing it and protein formation was encouraged, helping it cope with stress

In this article, Spencer et. al. observed the effect of the presence of endogenous Ghrelin on anxiety behaviour in mice. This data was obtained by running wild type and Ghrelin knockout-mice through a series of anxiety behaviour tests, as well as treating the knockout mice with exogenous Ghrelin following these tests and running these again. The focus of the research was on the anxiety behaviour displayed by the mice as well as the hypothalamic-pituitary-adrenal axis responses after acute stress experiences of the mice

Stress impacts the ability for children to learn and remember things due to the affect towards the brain, which can also impact them as adults. When a child is stress, the neurons, according to Eric Jensen, “generates a weaker signal, handle less blood flow, and processes less oxygen.” (9) The exposure to stress shrinks neurons in the brain’s frontal lobe. This is a crucial because if the frontal lobe is affected so is the prefrontal cortex, which is responsible for making judgments, planning, regulating impulsivity. The area of the brain that is being impacted is crucial for learning. Children experiences stress in poverty can cause, “impairs test scores, diminishes attention spans, and increases absenteeism and tardiness,” as Eric Jensen

On one occasion, they sorted mother rats into 2 different categories: highly attentive, and highly inattentive towards offsprings. After the pups of each groups grew into adulthood, the team analyzed their hippocampus (a brain region correlated to stress). Szyf and Meaney found in pups of inattentive mothers, genes regulating glucocorticoid (regulates stress sensitivity) are highly methylated compared to pups of attentive mothers. Methylated genes are harder to transcribe, causing behavioral changes in the pup's ability to manage stress. On another occasion, Szyf and Meaney gave pups born from attentive mother to inattentive ones and vice versa. Pups who were raised by inattentive mothers also showed methylation on glucocorticoid genes, supporting the notion that maternal care plays a large role on gene expression. Szyf and Meaney also mentioned that the timing of when the methylation happens is also important. Changes on gene methylation early on in life (0-2 years) showed stronger effects compared to middle age changes.

Mo, C., Renoir, T., & Hannan, A. J. (2014). Ethological endophenotypes are altered by elevated stress hormone levels in both huntington's disease and wildtype mice. Behavioural Brain Research, 274, 118-127. doi:10.1016/j.bbr.2014.07.044

According to animal studies, data shows that maternal stress in the prenatal stage may be directly related to cognitive impairments of offspring. This study examined whether psychological and endocrinologic measures of stress during human pregnancy predicted developmental outcome of the child at 3 and 8 months of age. The method used to collect data included collecting self-reported instances of hassle, anxiety related to the pregnancy, and salivary cortisol levels in 170 women. After birth, the children were followed up with. A decline of 8 points on the scale of mental and motor development was found due to stress on the mother. According to the study, stress causes a delay in motor and cognitive ability.

Repeated exposure to stress is manifested as allostatic load and disturbs the homeostasis of bodily functions. During stress, there is always an adaptive mechanism which restores the stress-induced deleterious effects on physiology and behavior. However, repeated uncontrollable stress leads to impairment in cognitive process. Chronic stress-induced effects are mediated by the hypothalamic pituitary adrenal axis (HPA axis). The HPA axis mediates the stress induced effects via enhancing circulating corticosterone levels. Excessive levels of corticosterone leads to impaired spatial learning and memory The HPA axis is regulated by hippocampus, prefrontal cortex and amygdala.

Stress, defined as a state where the homeostasis is disrupted and required subsequent adaptations, is a common phenomenon in today’s society (Kopin, 1995). It exists throughout the lifespan, starting as early as the fetal stage till one’s death. In particular, early life stress has come to light in recent years as it is becoming increasingly prevalent and more critically, it has been shown to increase the susceptibility to neuropsychiatric disorders, such as PTSD, in adulthood (Gibb et al., 2007). Since these psychopathologies are characterized by emotional dysregulation, especially in the aspect of fear as ELS has been associated with increased anxiogenic behaviors (Caldji et al., 2000; Ishikawa et al., 2015; Wei et al., 2010), it is important

The trouble begins when multiple life incidents hit us all at once and this is because during periods of dramatic changes, individuals are more vulnerable to stress (Jones & Bright, 2001). Therefore, stress has got the ability to activate pretty every system within the body, however, through a rather rudimentary mechanism which lies within the cellular level (Shreedhar et al., 2010).