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Stress is inevitable in life and “part and parcel of the human condition” (Powell et al., 1990). Although we are all familiar with the term stress as it is commonly used, the definition of stress remains blunt since it has become a term representing a complex group of concepts.
Over the years, many researchers from different scientific fields have focused on investigation of stress. As a result, stress has been defined by theorists in different ways: as an environmental stimulus, as a physical response, and as an interaction between environmental stimulus and the person (Selye, 1977; Mason, 1968; Lazarus, 1966; McEwen et al, 2003).
First introduced by Selye (1936), the term "biological stress" used to identify physiological responses in laboratory animals. However, he also recognized stress as processes, which people were involved into, trying to adapt and to respond to everyday life challenges. Thus, stress is a certain form of tension which occurs in organisms when exposed to external stimuli, which is followed by a certain pattern of psychological reactions. According to Selye (1977), regardless of the characteristic of the stressor, the one non-specific response-secretion of adrenal corticosteroids occurs following the stress. Selye also pointed out that although “stress” is necessary for life, “distress” must be diminished since it is harmful and unpleasant to the organism.
Contrary to Selye’s concept proposing that there is one non-specific response for all stressors, Mason (1968) showed that biological responses are stimulus-dependent and that both “physical” and “psychological” stimuli are capable of regulating adrenal cortical activity. Also, Mason (1968) emphasized that predictability, novelty and fear have massive influence on adrenal cortex responses.
A popular view was proposed by Lazarus (1993), who primarily focused on “psychological stress” and defined it, as “a relationship with the environment that the person appraises as significant for his or her wellbeing and in which the demands tax or exceed available coping resources”. According to his concept, the interpretation of the stressful event is more powerful than the event itself; more specifically, he proposed that stress is transitional, in that the occurrence of stress is dependent upon the degree to which individual percept conditions of the environment to be demanding, harmful and threatening. The cost of transition from one state of stress to another largely depends on the impact of external factors, either mitigating the cost of transition, or vice verse, making it greater.
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McEwen and Wingfield (2003) defined stress as “events that are intimidating to an individual and which draw out physiological and behavioral responses as a part of allostasis (the process of achieving stability through physiological or behavioral change), in addition to the ones, which are imposed by normal life cycle. They introduced two new concepts: allostatic load (i.e., adaptive responses to daily and seasonal, individual demands), and allostatic overload (i.e., the state in which the energy requirements exceed the energy income of the individual; or condition in which the organism continues to store energy, though energy requirements are not exceeded). In other words, stress can exercise valuable and positive impact in the form of mobilization of physical resources, necessary to meet demands, but also harmful effects in cases when the demands perceived are exceeding available resources of the individual.
For the purpose of this study, the concept of stress captures difference aspects of it that have been developed previously in order to assess the impact of emotional and procedural controllability on the general notion of stress, including different notions that it may encompass. Therefore, stress is defined as any threat, either real or perceived, to homeostasis (the tendency of an organism or cell to regulate its internal conditions, regardless of outside conditions). This, in turn, threatens the physiological or psychological integrity of an individual and results in behavioral, physiological, and/or endocrine responses (Selye, 1936; Mason, 1968; Lazarus et al, 1984; McEwen et al, 2003; Kalueff et al, 2004; Young et al, 2004; Vreugdenhil et al, 2001).
Effects of Stress
Effects of Stress on the Neuroendocrine System
HPA axis (hypothalamic-pituitary-adrenal) is a collective system of neuroendocrine units that regulate the adrenal gland hormonal activities in a form of a negative feedback network. The HPA axis activity is typically augmented by stressors and was found to be critically involved in the regulation of behavioral and physiological consequences of stress.
Exposure to a stressor activates the HPA axis, initiating a cascade of neuroendocrine events. This cascade includes the corticotrophin releasing hormone (CRH) discharge form the hypothalamus. Latter, in turn, is bonded to the certain receptors on cells in the brain's pituitary glands and induces the release of adrenocorticotropin hormone (ACTH) from the anterior pituitary culminating in the secretion of glucocorticoids (cortisol in humans and corticosterone (CORT) in rodent), into the circulatory system (Herman et al., 1997).
Circulating glucocorticoids then enable the organism to cope with the stressor and then return to pre-stress level of functioning. Thus, normal HPA axis functioning is essential for survival, maintaining bodily equilibrium. On the other hand, repeated activation of the HPA axis can produce damaging physiological effects and impair normal brain functioning.
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Effects of Stress on Other Systems
In addition to the psychopathological impact of stress on the health of people, there is evidence that stress has a considerable effect on the disease susceptibility such as heart diseases, poorer cancer prognosis, asthma, infection diseases and many more.
Acute and chronic psychological stress appears to impact differently on the immune system. Chronic stress can restrain various aspects of the immune system, while, at the same time, it is found that acute stress may have an enhancing impact on the immune system (Segerstrom & Miller, 2004). Genetic background, nature of the stressor, its previous history, as well as specifics of immune response generated are some of the interacting factors that determine the magnitude and direction of stress induced changes in disease outcome (Moyniham et al., 1996).
Effects of Stress on Learning and Memory
Various studies suggest that stress acts in many ways, so as to affect the processes that underlie learning and memory. Studies have demonstrated that arousing stimuli can exert profound and long-lasting effects on memory formation. Thus, while acute instance of stress can enhance memory formation in both humans and animals (McEwen et al., 1995), exposure to different stressors can impair memory and may induce amnesia. In other words, while brief period of stress can potentiate memory formation, prolonged stress may induce deleterious effects upon many aspects of cognition.
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Many of the hormones secreted during stress including ACTH, glucocorticoids, noradrenalin, etc as well as definite parts of the brain structure like amygdala. There is evidence in the literature that stress can considerably alter their role in the learning ability as well as memory processes (Akirav et al., 1999).
In particular, there are consistent findings in the literature that stress is considered to be a substantial biological factor that has an undisputable impact on the memory functioning in the hippocampus part of the brain. Amygdala is a brain area that is responsible for coordination of the behaviour during stress along with modulation of the memory consolidation. Also, it is a mediator of the stress effects on the memory as well as on the hippocampal long-term potentiation. On the physiological level, it is found that hippocampal slices exhibit impaired long-term potentiation from the stressed animals only while slices from the unstressed animals of the control group were showing opposite results. Moreover, those hippocampal slices from the stressed animals, which had amygdalar lesions, have exhibited normal long-term potentiation. Results of the study imply that an intact amygdala is needed, in order for the modulatory effects of stress on memory to be expressed entirely (Kim et al., 2001).
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Moreover, there are a lot of findings in the literature that glucocorticoid hormones are usually secreted following a stressful event. They have a considerable impact on the cognitive performance in the stressful environment (learning ability and memory capacity). Even though several studies have found a positive impact of stress on the cognitive ability, majority of the research finds evidence that glucocorticoids have impaired effects on memory capacity during stress. According to Roozendaal (2002), impact of stress upon the memory capacity and, consequently, the learning ability, depend mainly on the phase of the learning process. Activation of the glucocorticoid-sensitive pathways that involve receptors of glucocorticoid in the post training phase usually enhances consolidation of memory. On the contrary, learning and memory processes are impaired in situations with high circulating levels of glucocorticoids. Moreover, this is the case after infusions into the hippocampus of glucocorticoid receptor agonists. Therefore, it is found that stress may have dubious impact on the learning ability as well as memory processes depending on the phase of the latter (Roozendaal, 2002).
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Hence, even though there is no consistency in the literature about the degree and direction of stress impact on memory and learning ability, it is found that biological processes as well as various hormones that are secreted during stressful even may considerably alter learning capacity, either impairing it or enhancing further.
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