Hippocampal Dysfunctioning Essay

Cortisol plays a major role in the development of this disorder. It is secreted by the adrenal gland, located above the kidneys, in a precise sequence of events. The hypothalamus directs corticotropin-releasing hormone(CRH) to the pituitary gland.1 CRH causes the pituitary to release adrenocorticotropin hormone(ACTH) activate the adrenal glands.1 The adrenal glands pick up the ACTH, they reciprocate by releasing cortisol in the bloodstream.1 Cortisol helps with quite a few of your body functions. Some of these functions are stress response, balancing the effects of insulin, reducing the immune system’s inflammatory response, regulating

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Some researchers hypothesize that the hippocampus is involved in some types of memory processes but not others. This particular study measured brain activity using fMRI during two types of memory tasks: remember (episodic memory) and know (familiarity). A memory was considered “episodic” if the person could recall the moment it was learned and “familiar” if they felt they recognized the word but could not retrieve the specidic moment it was learned. The a priori (pre-selected) region of interest( ROI) in the hippocampus

The hippocampus, which is the Latin word for seahorse, is named because of the shape it holds (Hippocampus). It is the neural center in the limbic system (Myers, 368). This system is located in the temporal lobe, close to the center of the brain. The hippocampus is essentially involved with the storage of long-term memory, especially of past knowledge and experiences (Hippocampus). The hippocampus is also vitally important to the creation of new memories, and without it humans would always be living in the past.

What is the hippocampus? The hippocampus is the formation of memories and a part of the cerebrum.Some people say if you damage the hippocampus you develop a disease called Antevograde amnesia which is the unibaily to form new memories.It also said there are regions that regulates the emotions.

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

GCs use the hippocampal neurons vulnerability to impair their energy metabolism. The neurons are affected greatly to such disruption. GCs affect energy production or pathologically increase energy consumption. GCs prevent glucose to be utilized in the hippocampus. GCs have proved to damage neurons of the hippocampus by using pharmacologic (branch of medicine concerned with the study of drug action)GC concentrations. Long term exposure to high levels of glucocorticoid increases the aging process of the hippocampus. The damage is most likely elevated from high concentrations of GC receptors known as (NR3C1) this represents Nuclear receptors subfamily 3, group C, member 3, their receptors found in the hippocampus. No studies show that the “GCs can be directly toxic to the hippocampal neurons. However, recent work suggest that GCs can induce a state of vulnerability in these neurons, which are then less likely to survive a broad range of metabolic insults”(Robert M. Sapolsky). GCs could harm or damage the hippocampus even at is below average concentration. The GC action is to inhibit of glucose uptake to the surrounding tissues. This action of glucocorticoids

The hippocampus lies near the center of our brain. It's functions include storing our memories and maintaining a hormone called cortisol. During the time of physical and mental stress, our body releases immoderate amount of cortisol that can create chemical imbalance in the body and cause problem. During depression, long term exposure to increased cortisol level in dentate gyrus (a part of hippocampus) cause hippocampus to shrink as well slow down the production of our neurons. This can lead to memory

Under conditions of stress, the nervous system, via the SAM (sympathetic-adrenal-medullary) and HPA (hypothalamic-anterior pituitary-adrenal cortex) systems, produces neurotransmitters and hormones (such as cortisol and catecholamines) that bind to receptors on immune system cells;

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.

There is a circuit of structures that form a functional route of communication of emotions in depression. These structures surround the brainstem (the cingulate gyrus, hippocampus, the hypothalamus, and the anterior thalamic nuclei). The use of MRI, PET and fMRI technologies establish the understanding of the malfunction of the limbic system being central to the pathophysiology of depression. The prefrontal cortex (PFC) plays a role in regulating autonomic and neuroendocrine responses, pain modulation, aggression and sexual behaviors. PET studies have shown abnormalities in cerebral blood flow and glucose metabolism in multiple prefrontal cortical and limbic structures implicated in emotional processing. The amygdala are involved in recruiting and coordinating cortical arousal and neuroendocrine response to underdetermined stimuli as well as in emotional learning and memory. Abnormal activation of the amygdala results in severity of depression and is also linked with bipolar depression and anxiety. The hippocampus plays a fundamental role in learning and memory, and its is rich in corticosteroid receptors. Dysfunction is the hippocampus is responsible for inappropriate context-dependent emotional

The hypothesis of the effect of exercise training on hippocampal volume in humans: A pilot study was compared to aerobic fitness with older humans to examining if the earlier study was correct. The study was to find out if aerobic exercise training can increases hippocampal volume with older adult. (Parker, Beth A; Thompson, Paul D; Jordan, Kathryn C; Grimaldi, Adam S; Assaf, Michal; et al. Research Quarterly for Exercise and Sport 82.3 (Sep 2011): 585-91.) Hippocampal volume is a brain structure below the cerebral cortex of the brain. Hippocampal volume is important because it process information and formed memories, organizing information and concentration. (What Is Hippocampal Volume?, 2017). The sample chosen for this study adequate was animal. The reason why animal was used in this study because studied have shown there is convincing evidence that exercise training increases hippocampal volume.

Corticosterone is formed in the cortex of the adrenal glands. For many animals, corticosterone serves as a glucocorticoid. A glucocorticoid is a type of steroid hormone that moderates metabolism of glucose. Glucocorticoids are commonly known as stress hormones. Therefore, corticosterone is a hormone that is utilized to regulate immune reactions, stress, and energy. Corticosterone is similar to cortisol, a glucocorticoid that is effective in humans. Corticosterone is more effective in non-human animals like reptiles and amphibians; the hormone can inhibit protein synthesis. If an animal is exposed to too much of a hormone, the animal can face detrimental effects. For example, if a bird were to encounter too much corticosterone, it would become more aggressive as it grew. After doing some research on this hormone, I discovered that corticosterone is commonly used in research to induce stress on test subjects. Khalid’s research lead mice into a corticosterone-induced depression in order to further analyze brain pathways when experiencing depression. To me, it is extremely interesting that chemicals within the body can alter our state of

“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).

S. F. Sorrells, J. R. Caso, C. D. Munhoz, and R. M. Sapolsky (2009) ?The stressed CNS: when glucocorticoids aggravate in?ammation,? Neuron, vol. 64