Antidepressants Lab Report

In this article, antidepressant medication (ADM) is described as the most commonly used treatment for severe depression and cognitive therapy (CT) is the most talked about treatment that could be used for severe depression. Although, some patients do not want to take ADMs daily and CT is still being studied as a treatment option for major depression disorder. There was another alternative therapy treatment that was being questioned, behavioral activation therapy. The primary objective of this study was to test the effectiveness of behavioral activation therapy towards adults with major depression disorder. For this study, behavioral activation was studied with cognitive therapy and antidepressant medications in a placebo controlled randomized

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 hippocampus is smaller in patients with depression. The smaller hippocampus is thought to be diminished because of a persistent exposure to stress hormones, like cortisol, which impacts the growth of nerve cells. The hippocampus is highly susceptible to stress, perhaps because the protracted ontogeny or the high amount of glucocorticoid receptors (Uma Rao et al.; 2010). The longer the patient has depression, or the more episodes of depression the patient experiences, the smaller the hippocampal volumes become. Stress correlates with the smaller hippocampus, researchers used twenty-nine patients with depression, twenty-two patients with severe depression and thirty-two control patients. All patients were around the same age, physically healthy, alcohol and drug free, and did not have any other kind of mental illness like bi-polar disorder, autism, or schizophrenia. Structural imagery was used to obtain the images of each patients’ entire brain. Then an image was aligned with the anterior commissure and posterior commissure as well as the borders of the left and right hippocampus. From the MRI scans and using a formula the hippocampal volumes were figured. All of the patients were followed up on, every 6-months for up to five years. The results were conclusive, the severely depressed and the depressed patients had smaller hippocampal volumes when compared to the control subjects. The left hippocampus of the patients was smaller by 4.9% and 4.2%, respectively, while the

Given that socio-environmental chronic stressors influence the development of depression, stress-based animal models have been used to explore biological mechanisms of this disorder. Unpredictable stressors have a greater negative impact than predictable stressors due to their uncertainty (Bondi et al., 2008). Therefore, unpredictable chronic mild stress (UCMS) has been developed as an experimental model of depression. Converging evidence has shown that UCMS induces anhedonic-like behavior in mice (Mineur et al., 2006), but little is known about the neurobiological mechanism of the abnormal behaviors caused by UCMS.

What is more, several metabolomic studies to investigate drug response on patients with a chronic mild stress (CMS) model of depression were performed. One of these, conducted by Zhao and colleges, identified biochemical changes induced by two widely used anti-depressants: fluoxetine and imipramine [83]. Metabolic profiling of hippocampus of C57BL/6J mouse by gas chromatography-mass spectrometry

From the study, different possibilities of the IFN- α caused depression were mentioned. One of them is that IFN-α may caused depression by reducing tryptophan availability which can make IFN-α-induced depression resistant to SSRIs. In addition, levels of serotonin transporter mRNA is increased by treatment with IFN-α (1).

Stress is one of the most major factors responsible for depressive disorders [1,2]. The chronic mild stress (CMS) model, a widely used rodent model of depression, consists of repeated exposure to various of unpredictable and mild stressors and it. And it has been shown a decrease in reward sensitivity in various behavioural paradigms [3] induces changes in hypothalamic-pituitary-adrenal (HPA) axis [4,5] but also of other biological and behavioural markers of human depression, including architectural sleep abnormalities[6,7] disturbances in circadian rhythms related to locomotor activity[8]using of variety of drug treatments during the application of stress can be reversed these disturbances

The amygdala is a critical substrate or a pair of critical nuclei within the subcortical limbic system regulating emotion- and mood-related behaviors. Further, the nerves connected with multiples of other structures involved in stress responses, including, the prefrontal cortex (PFC), the mesolimbic reward pathway and the hippocampus. The amygdala activates the natural flight or fights to escape from dangerous situations, learning to fear and not to fear, creating memories of fear and safety. According to ….. Studies show that numerous structural and functional neuroimaging methods have revealed activity-dependent adjustment of the amygdalae for hyperactivity and hypertrophy in patients with psychiatric illness. Similarly, the current study in rodents shows that three hours per day of restraint stress for 14 days cause mice to show long-term depressive behaviors, manifested by disrupting sociality and despair levels of extracellular glutamate. And that chronic restraint stress-provoked hypertrophy of BLA neurons can be reversed by lithium treatment; implying that stress-related abnormal remodeling of BLA neurites can be medically reversed in chronic stress-related disorders. These behavioral changes communicated with

Gone grocery shopping but forgot what it was you were even looking for? When serotonin levels are low, we may have difficulty concentrating or experience anxiety; stress can also induce mental burn-out, causing serotonin levels to plummet. In more severe cases, we may exhibit decreased self-esteem and bouts of melancholia. It is for this very reason that classical antidepressants focus on manipulating serotonin levels, by either stimulating the brain to produce more of those “happy juices” or by boosting its sensitivity so that neurons respond better to existing

Depression consequences from abnormalities within the interactions among neurotransmitters and hormones within the mind, including the hypothalamus-pituitary-adrenal (HPA) axis; noradrenergic, serotonergic, and dopaminergic structures; neuropeptides; and brain-derived neurotrophic aspect (BDNF), and might cause structural modifications in the brain.

Stress is one of the most important factors responsible for depressive disorders [11]. The chronic mild stress (CMS) model, a widely used rodent model of depression, consists of repeated exposure to an array of varying and unpredictable, mild stressors and it induces changes in hypothalamic-pituitary-adrenal (HPA) axis Katz et al. 1981Vollmayr B, Henn FA (2003)

The cells of the hippocampal formation are very sensitive to the effects of stress and the serotonin neurotransmitter protects against stress and ultimately depression. An experiment was conducted to test if stress causes depression by the decreasing number of pyramidal cells of the hippocampus (Praag et al.; 2000). Removing a non-stressed rats’ adrenal glands resulted in an increase in neurogenesis in the hippocampus. This is due to the removal of cortisol, which is normally released from the adrenal glands based on the hypothalamic-pituitary-adrenal axis. Glucocorticoids the stress hormones that are released from the adrenal glands; therefore, without the adrenal glands there is less cortisol acting at the hippocampus and preventing the neurogenesis. The

According to Morgan (2015), the neuroscience of depression has an emotional impact on many areas of the brain. The stressors in the hypothalamus pituitary adrenal axis initiate the release of the

: According to mechanisms of inflammation- associated depression which cytokines plays a major role in progression of these disorders open new possibilities for developing anti-inflammatory drugs or new anti-depressant compounds targeting neuroinflammation or its pathways. Also an effective strategy for detecting depression in the early stage can prevent neuroinflammation subsequently neuroinflammatory

Interestingly, both tricyclic and SSRI antidepressant drugs commonly used to treat depression reverse the behavioral changes induced by ZnD indicating the feasibility of ZnD animal models in the study of depression.