The Effect Of Acute Administration Of B Carboline Harmine On The Behavioral And Physiological Of Rats Exposed From Cms Procedure Essay

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”

stress and to relieve anxiety varies from one person to another” (p. 1). The author

A test done by Robert Sapolsky form Stanford University shows how anxiety can escalate to depression through subjecting rats to electric shock. The shocks occurred periodically and the rats soon learned that to stop the shocks, they had to press a lever. Once that was learned, the rats were seen to be constantly alert, waiting for the shocks to occur. However, the next time they occurred, the levers were disable and the rats repeatedly pressed it, hoping the shocks would stop. After a while, they realize that their efforts are futile and went into despair, which is measured through the levels of dopamine, serotonin and noradrenaline (norepinephrine) in their brains. (SCI. AMERICAN)

Stress and anxiety affect a large segment of the child and adolescent population. Numerous stressors from a wide range of domains contribute to the current levels of subclinical anxiety and diagnosed anxiety disorders. Without effective coping strategies, the cumulative effect of these stressors can lead to the clinical diagnosis of one or more anxiety disorders. Left untreated, these disorders can carry severe long-term consequences, including social, cognitive, and academic impairments. Furthermore, these deficiencies can lead to significant limitations in adulthood, such as reduced career choices, substance abuse, and an increase in the use of both mental and physical health care.

Although the understanding of mTBI pathophysiology is incomplete, it is suggested that anxiety disorder have generally linked to the abnormalities in the amygdala and prefrontal cortex (1). As a result, multiple animal models have been used to test different behavioral outcomes to evaluate the pathological effects cause by the injury model (4). While other experiments test anxiety behavior by exposing rodents to varying conditioned stimuli like electric shock or loud noises, the elevated plus maze (EPM) rely upon unconditioned fear of height and open spaces (P). Thus, the elevated plus maze is normally used to assess rodents’ innate anxiety (4). EPM also facilitates in assessing “anxiogenic drugs” as well as “anxiolytic drugs” of multiple pharmacological agents. However, methodological differences in “age, strain, or sex of the subjects includes housing or testing conditions” often attribute to the inconsistent outcomes (4). In this experiment, EPM is the primary animal model use to determine anxiety levels in induced repetitive mTBI female mice as compared to sham

Human beings are susceptible to high levels of stress and anxiety in today’s world. Monetary needs and challenges presented by uncontrollable circumstances contribute to increasing stress-like symptoms for people

The discovery that selective serotonin reuptake inhibitors can effectively treat anxiety disorders has led to the Serotonin Theory. The Serotonin theory indicates that serotonin mediated neurotransmitters in the brain may be involved in anxiety disorders. The fact that some antidepressant agents relieve symptoms of both anxiety and depression disorders indicate that there may be a correlation between the two disorders. Information also indicates a correlation between genetic susceptibility in depression and anxiety disorders (Lundbeck Institute, 2008.)

A recent article from BigThink, written by Philip Perry, discusses a group of researchers who have found the source of anxiety within the brain. Mazen Kheirbek, Ph.D, the head researcher of this study, stuck a miniature microscope in the brains of mice in order to find what he is now calling “anxiety cells”. Kheirbek put the mice in strenuous situations that would cause them to have anxiety, he then looked for the part of the brain that had the most activity; thus he was able to find the location of the cells. This new discovery is a big step in creating better medications for anxiety sufferers. Current anxiety medication prescribed by physicians are only partially effective at controlling anxiety; Kheirbek states that medication that can

The independent variable in this experiment was whether the rat was raised in isolation with no toys or in group with toys and which cage they were tested in whether it was the home cage or a new cage. The dependent variable was how many times rats in each scenario stuck their noses in the candles flame. Results showed that almost every rat stuck their nose into the flame in pure curiosity however, rats raised in a restricted environment and placed in a new environment stuck their noses in almost double the amount of times than any other rat did. These results indicate that rats raised in isolation handle stress differently and that those in isolation have poor pain avoidance. I liked this study because it shows that curiosity is prominent in rats as in humans although it only takes us one time to realize something hurts to not do it again. It also shows that something raised in isolation reacts to stress in a negative way and proceeds to harm themselves and with this evidence we can maybe understand why depression can lead to

This was regulated for 10 minutes which was actuated by putting the mouse in a slender space in a vinyl sack with breathing holes; this test was performed once per day for four days. Histone deacetylase sodium butyrate and valporic acid, selective CB1 agonist ACPA, and selective CB1 opponent SR was directed for 30 minutes before every nicotine and immobilization stress treatment. The control group did not get any medication or stressor treatment, a mixed solution of DMSO and distilled water was infused and in addition saline as opposed to the nicotine, immobilization stress and CB1 treatments. Anxiety related behaviors were analyzed in the elevated plus maze test which utilizes a cardboard contraption that comprised of two inverse open arms and two encased arms. The assessments of the parameters were performed at the 2 hour time point after the last nicotine and immobilization stress treatment. Depression related behaviors were inspected in the forced swimming testing which utilized a glass cylinder apparatus containing water at 21-23°C with an infrared sensor set over the

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 tripartite model, unlike the status quo, “posits that in addition to the common factor of negative affectivity there are specific components” of depression and anxiety that can better differentiate between the two. These specific factors, which were incorporated into the items of the PANAS by Watson et al (1988), include physiological hyperarousal and low PA (anhedonia). To test these predictions, Watson & Clark (1991) administered the Mood and Anxiety Symptom Questionnaire (MASQ), a questionnaire consisting of three depression and anxiety scales as well as two more specific scales, to multiple student, adult, and patient samples. The results of this study revealed that the specific measures had extremely high discriminant validity compared to the general measures, supporting the validity of the tripartite model. As a result of its foundation in the tripartite model, the PANAS has been shown to be effective at differentiating between depression and anxiety in clinical samples, which explains why it is largely utilized in clinical settings (Dyck, Jolly, and Kramer, 1994). Additionally, a study by Crawford & Henry (2004) evaluated the relationship between the PANAS and other measures of anxiety and depression (HADS and the DASS, respectively), revealing that the PANAS has high convergent validity with measures

An examination of the conditions endured by research animals beforehand can also be attributed to a source of conclusion inaccuracy between animal experimentation successes and clinical research failures. Stress, commonly experienced by animal subjects in a lab setting, is a major factor known for contaminating the accuracy and reliability of biomedical research results. Stress causes a chain reaction of heightened readings, such as increased heart rates, pulses, muscular actions, and hormonal balances. Executing experiments on a subject with misrepresentative vital signs can greatly skew the results and interpretations drawn from a study. Stress can be experienced in a variety of manners. Mice, for example, experience a reactive condition known as “sympathy pains” when in a laboratory setting. In addition to the individual response taken at the foreign sights, sounds, and smells, mice are affected by the stress level and anxiety experienced by other mice surrounding them. Like humans, mice can feel sympathy towards one another and react accordingly. Performing experiments on animals that suffer from an abnormal amount of stress will skew evidence collected, and make it difficult for scientists to reach conclusions about predicted similar human responses.

INTRODUCTION: Even though stress negatively affects physical and mental abilities. Stress is the cause of tensions, overwork and increasing demands. Generally, the Anxiety is a part of our life. We live with it, manage it, or more all stress over it. Our lifestyle, the region in which we live, the economy, and our occupations can result in a lot of anxiety. Not everybody manages the same level of anxiety and there are a few elements that can affect our lives and reason us to have higher or lower anxiety levels. (Feldman, 2009)

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