Mild Stress Theory

Immune System: When people are under intense stress for a while, their immune systems may become dysregulated, leading to lower functioning of important white blood cells called lymphocytes and to increased production of C-reactive protein (CRP), a protein that spreads throughout the body and causes inflammation and various illnesses. Some studies suggest that immune system dysregulation of this kind may help produce depression.

“The ‘stress hormone’ cortisol is believed to create a domino effect that hard-wires pathways between the hippocampus and amygdala in a way that might create a vicious cycle by creating a brain that becomes predisposed to be in a constant state of fight-or-flight” (Bergland, 2014).

Animals and Humans have a biological stress response intended to facilitate survival in the case of a life threatening attack or severe illness. This is commonly referred to the “fight or flight” response. Some primates, including humans have developed the unhealthy propensity to trigger this response for psychological or social reasons. Humans in particular experience the stress response exponentially more often for psychological reasons than for the purpose of survival (Stress, 2008). For example, we are may feel “stressed out” about work or school and if we think about it too much and get upset, we may experience a stress response Just by thinking about something that is bothering us, we can trigger the biological “fight or flight”

The depression diseasing our society today is mostly caused by stress related activities. Because our society demands so much out of us we struggle to handle all the stress it throws out us. STanford researchers found people who had depression had smaller hippocampuses; the part of the brain that controls long term memory and emotions. The researchers also found that this smaller hippocampus was caused by a deterioration of it over time, not in one sudden moment. THe deterioration is caused by, you guessed it, stress. However, it’s a double edged sword, because as stress causes the deterioration, it also prevents the healing process by preventing neurons from growing around the

Psychology, as most know, is the study of the mind and personal or group thoughts, feelings, and emotions in humans and animals. Scientists study, analyze, and investigate many areas of psychology, but the causes and effects of mood disorders and emotion irregularities are still unrecognized. Many studies were an attempt to find more information on mental illnesses. One of the most common illnesses in the United States is depression, also; it is the most often recognized mental illness in the world. What most clinicians don’t know, however, is what happens in the brains of patients before, during, and after depressive episodes.

Through my research, I’ve learned that in terms of depression, there are three major parts of the brain that play a significant role in the illness: the amygdala, the hypothalamus, and the hippocampus. The limbic system, as a whole, and other parts of the brain are also involved when dealing with depression. However, the amygdala, hypothalamus, and hippocampus are three parts that show up most commonly when researching the effects of depression on the brain. The amygdala – like the other effected parts of the brain – is part of the limbic system, which is a set of structures in the brain that controls actions and emotions that ensure survival. The amygdala is primarily associated with emotions like anger, fear, pleasure, sorrow, and sexual arousal. Activity in the amygdala is higher when sad or depressed. The hypothalamus acts to regulate things like body temperature, appetite, sleep, sex drive, stress reaction, aggressive behavior, reactions to pain, and it helps control the pituitary gland – which regulates hormone control. When dealing with depression, the hypothalamus is prone to hyperactivity. Finally, the hippocampus’ role in the brain is to make short term memories into long term memories. It also plays an important role in spatial navigation. In depressed people, the hippocampus is generally smaller than those not suffering from depression. Brain activity, as a whole, is generally lower in people suffering from the

Although many studies have shown that impaired neurotransmission of serotonergic and dopaminergic pathways are related to depression [2], the pathophysiology of depression is yet to be fully elucidated [3]. Several studies are being conducted to unravel the underlying mechanism in evaluating the therapeutic efficacy of antidepressants [4,5]. More so, chronic stress exposure has been found to cause atrophy of neurons in rodent hippocampus. [6,7] As such, decreased hippocampal plasticity might be closely connected to depression. Recent studies have found that administration of antidepressant agents to either stress-induced models or patients could heighten developed neurons in the hippocampus, which in turn attenuates the depression symptoms [8,9]. Researches have demonstrated that the expression of SYP is reduced in brain of depressed patients, suggesting a correlation to the pathophysiology of depression [10,11]. Brain magnetic resonance imaging shows that hippocampal volume is significantly smaller in patients with depression compared with normal control [12]. In vitro experiments have also established that depression ensues along with high levels of cell apoptosis as well as increased protein level of Beclin 1 and LC3 [13, 14]. Thus, apoptosis and autophagy

There has been a myriad of research investigating the symbiotic relationship between hippocampal volume and major mood disorders (MDD) like depression. Despite being one of the most prevalent illnesses, the underlying pathogenesis and neurobiology of MDD remain unclear. It has been widely documented that patients with a MDD tend to have smaller hippocampal volumes (Sheline et al., 1996, Nordanskog et al., 2014). The hippocampus is known to be closely affiliated with the hypothalamic-pituitary-adrenal axis, which is required to produce glucocorticoids that are involved in stress mechanisms (Chen et al., 2010). Moreover, stressful life events are considered a critical risk factor in the development of depression (Zannas et al., 2013). This, coupled with findings which suggest that depressed patients have difficulty with hippocampal-dependent learning and memory tasks (Gould et al., 1998, Gould et al., 2007), accentuates the relationship between the hippocampus and MDD being mediated through stress. There are various hypotheses regarding what may cause hippocampal volume diminution as a consequence of stress. Major propositions involve hippocampal neurogenesis in the dentate gyrus (Becker and Wojtowicz, 2007), glial numbers, apoptosis (Czeh and Lucassen, 2007) and granule neuron numbers (Boldrini et al., 2013). Other mechanisms that may affect hippocampal volume like neuropil reduction, shifts in fluid balance between the ventricles and brain tissue and changes in

The physiological and behavioral effects of early life stress (ELS) on the developing and adult brain are a subject of great interest in the field of neuroscience today. The ability to delineate the mechanisms and structures that are affected during postnatal exposure to chronic stress has the potential to provide invaluable insight into the development of a multitude of neuropsychiatric disorders. While we have come to understand a few of the mechanisms involved in many of these illnesses – such as the significance of the serotonin (5-hydroxytryptamine, 5-HT) neurotransmitter in many depression cases – the complex nature of these disorders and our ability to effectively treat them remains elusive. Such an understanding of how the brain adapts and differentially develops as a result of chronic stress, particularly in early life, may also be able to broaden our understanding of the way in which the brain codes and responds to a variety of emotional triggers.

Biological and neurobiological studies have become more and more closely correlated with mental disorders throughout the past decade of scientific progress. This paper aims to expound models that have contributed to our developing understanding of the origins of Major depressive disorder (MDD) and treatment guidance, from both neurobiological and biological fields. It will also explore the implications, both positive and negative, for societal and personal integration of the knowledge that these advancements provide.

A deficiency in both serotonin and norepinephrine neurotransmitters specifically in the locus coeruleus, and the dorsal raphe nucleus, which both are important in relations to serotonin receptors can cause depression in AD. Individuals who had both AD and depression showed fewer neurons in the two locations when compared to non-demented individuals (Modrego, 2010 as cited by Zubenk, Moossy & Knopp, 1990). The use of animal shows the links of depressive behavior and AD. Ledo et al. (2016) used a mouse model to show an association of amyloid beta oligomers (AβOs) and depressive like behavior. It was hypothesized that AβOs induced depressive behavior in AD by causing an inflammatory response, which was triggered by activation of microglial cells. Ledo et al. (2016) found that AβOs decreased serotonin levels in the mice. This suggest that the decrease levels in the brains are leading to abnormalities in the AβOs, which then causes cognitive impairments.

The PVT has shown to have implications in stress processing due to its diverse population of neurons, holding a variety of functions. People are still discovering more about the PVT and its roles, but it is important to be able to categorize the neurons directly involved in stress. To discover more, I worked with c-fos, a protein which is a promoter for previous neuronal activity for the two restraint-stress experiments. For the first experiment, I used immunohistochemistry to label neurons expressing c-fos in both control and restraint mice. The raw data shows that with restraint there is an increase of c-fos expression in the PVT. In addition, the stainings show that there are two groups of neurons activated during times

Discrepancies between 5-HT1AR mRNA and protein expression levels in different brain regions have been reported in animal stress models. Iyo et al., 2009 observed increased 5-HT1AR mRNA level and decreased protein level in the PFC [6]. Our earlier animal studies showed no changes in 5-HT1AR mRNA in the PFC of female rats subjected to prenatal stress, in pregnant stressed female or in the Hp of male rats subjected to chronic mild stress [15]. However, 5-HT1AR protein levels were reduced in these groups of rats [15]. Shishkina et al., 2012 [12] reported an increase in 5-HT1AR gene expression in the PFC of rats exposed to FST; this effect was reversed by chronic fluoxetine treatment [12]. However, in the non-stressed rats, fluoxetine

Eiland, L., & Romeo, R. D. (2013). Stress and the developing adolescent brain. Neuroscience, 249, 162-171.

There is a very complex relationship between stressful situations, our mind and body’s reaction to stress and the onset of depression. Some people develop depression after going through stressful events in their lives, such as the death of someone close, loss of job and other negative and traumatic problems that can cause large amount of stress (Prentiss, 2009). These problems make us experience a mixture of physical and emotional effects that can create stress as a positive or negative feeling. The human body is designed to experience and react to stress; it can be both a positive and negative influence. Positive stress can give a person the drive and