Brain Functions in Depression - Coursework Example

Brain Functions in Depression The increasing number of antidepressant users proves that depression is on the rise. This paper uses theories of depression to illustrate the causes of depression from a Biopsychology issue. These arguments will show the functions of the brain that cause depression and the changes in the structural brain due to depression. This essay will ensure the reader understands the major complications involved in the brain and ways that antidepressants can reduce depression. Depression is one of the major forms of mental health in the current world. There is a rising number of antidepressant users due to increased stress that is due to economic constraints and poor eating habits. The brain handles mood and emotional control, thus the need to tackle the theories on depression that portray the causes and effects of depression by addressing the inability of the brain to limit stress. The causes of depression are many as several theories illustrate. There are claims that depression that causes mental health can be genetic or due to environmental stress brought by life hardship. Other sources claim that depression is due to the imbalances of biogenic amines in the brain (Farooqui, 2010). These claims have some bearing since the brain is one of the most researched parts of the body. In all the claims, the brain is the center of the causes of depression since it handles controlling emotions, sleep, mood and other desires, for instance, sexual desires. The brain controls all the functions of a human. The brain is the determinant of depression. The aim of this essay is to determine the truth of the various theories that portray the brain as the cause of depression. The essay will analyze the structural brain changes in depression examining the truth behind the claim that imbalances of one or more biogenic amines in the brain are the cause of depression. Moreover, the essay will tackle the issues that make the brain structures change their functions, thus leading to stress and depression (Chang, 2012). The article uses various theories to portray the importance of receptors and neurotransmitters in determining mood control and emotional behaviors. The Brain Control of Mood and Emotional Behaviors Different approaches illustrate various causes of depression. Pathophysiology of depression suggests that depression is due to disturbances in the brain’s central nervous system (CNS) where neurotransmitters, for instance, serotonin, norepinephrine, and dopamine are affected. The role of CNS serotonin activity is acting as a major depressive disorder that limits the efficacy of selective re-uptake inhibitors. Serotonergic neurons implicated in affective disorders are found in the dorsal raphe nucleus, the limbic system, and the left prefrontal cortex. Vascular lesions also contribute to depression since they disrupt the neural networks that are involved in emotional regulation (Farooqui, 2010). Depression, mainly affects the limbic circuitry where the hippocampus and amygdala are found. The functional neuroimaging studies support that depression is due to decrease metabolic activities in neocortical structures, therefore increasing metabolic activity of the limbic structures. The need to determine the part of the brain that is abnormal during depression led to scientists and neurologists use positron emission tomographic images (PET). They discovered that the prefrontal cortex had abnormally diminished activity with patients suffering from unipolar depression and bipolar depression (Farooqui, 2010). This region controls emotional responses and connects to other areas of the brain. The functioning of these structures are controlled by neurotransmitters such as noradrenaline, serotonin, and dopamine that most scientists believe that they control mood and emotional behaviors. Norepinephrine is synthesized from the dietary amino acid tyrosine in the locus cerulean in the mid-brain. The axons of these neurons project upward through the forebrain to the cerebral cortex, the limbic system, thalamus and the hippocampus. This neutron is believed to be one of the key neurotransmitter involved in the control of mood and emotional behaviors, for instance, anxiety, aggression, stress and sleep patterns (Chang, 2012). Presynapse and binds release noradrenaline to receptor sites on a postsynaptic neuron. The residual noradrenaline is recycled into storage vesicles or metabolized by the enzyme monoamine oxidase. Serotonin and serotonergic system originate in the raphe nuclei of the brainstem and projects to the cerebral cortex, limbic system, cerebellum and the spinal cord. Serotonin regulates pain, pleasure, anxiety, panic, arousal and sleep behaviors. These transmitters being the determinants of mood control and emotions form the basis of several hypotheses or theories of depression (Farooqui, 2010). Theories of Depression Several methods determine the causes of depression. These theories are; biogenic amine hypothesis, receptor sensitivity hypothesis, and the permissive hypothesis among many others. The Biogenic Amine Hypothesis These are one of the oldest methods since it was realized back in the 1950s, claiming that drugs that decreased monoamines precipitated depression whereas those that increased monoamines relieved depression. This theory states that the deficiency of monoamines causes depression mainly noradrenaline and serotonin. Blocked monoamines, neurotransmitters are not metabolized; thus antidepressants handle inhibiting monoamine oxidase (MAO) (McLeod, 2015). These drugs may also limit the uptake, therefore preventing the presynaptic neuron from reclaiming neurotransmitter, hence increasing neurotransmitter in the synaptic cleft. The Receptor Sensitivity Hypothesis The rise of neurotransmitter in the synaptic cleft increases the stimulation of receptor sites, thus prompting the postsynaptic neuron to compensate by decreasing receptor sensitivity. This process of desensitization. This hypothesis claims that depression is a result of pathological alteration or super-sensitivity and up a relationship with receptor sites. Depression is due to too little stimulation by monoamines caused by the deficiency of noradrenaline and serotonin in the synaptic cleft (Chang, 2012). This theory provides an understanding that is missing in biogenic amine hypothesis on the reasons behind the long duration taken after consuming antidepressants. It claims that antidepressants reduce the receptors super-sensitivity, hence the long length of the work. The Permissive Hypothesis This theory states that a balance of serotonin and noradrenaline and not absolute levels of these neurotransmitters or their receptors control mood and emotional behaviors. It claims that the small central serotonin function inhibits a range of neurotransmitter functions. These low levels of serotonin lead to an abnormal increase of noradrenaline causing depression or mania. In a situation where the serotonin cannot control noradrenaline, it leads to declining of the latter causes of depression and vice versa. Antidepressants regulate the levels of the two neurotransmitters, thus relieving stress and depression (Chang, 2012). Discussion The above theories, although they are not perfect illustrate that depression is due to abnormal levels of either noradrenaline or serotonin making the statement true. The second part of this paper is to discuss the brain function in any depression since it is a contentious issue. Depression changes the structure of the brain, and the changes or remodeling that is preventable and is reversible with the right medication (Townsend, 2014). Earlier brain images of depression patients indicate that there were changes in the brain area involved with mood, memory and decision making since the brain functions in response to the depressive episodes. The primary structures that change are hippocampus, prefrontal cortex, and amygdala since they handle identifying the stressful event and generate a response to the situation. The hippocampus stores memories and controls the production of new neurons, thus stress slows down the dentate gyrus making neurons in the hippocampus shrink. The changes are similar to the effects of depression on the prefrontal cortex, but in the case of amygdala, becomes more active in the event of depression thus enlarges. The enlarged hyperactive amygdala and the abnormal activities in other brain structures leads to sleep disrupted patterns. It affects secretion of hormones and other chemicals in the body, hence weakening the physicality of the depressed patient (Townsend, 2014). Conclusion The paper discusses the main neurotransmitters that handle the control of moods and emotional behaviors. These neurotransmitters are mainly serotonin and noradrenaline that should be normal to ensure a person is not depressed (Farooqui, 2010). The theories of depression are interrelated, since they focus on the abnormal monoamines processing that makes it hard to control the mood and emotional behaviors. The external environment affects the essence that the theories have not indicated the relationship of external effects as a cause of the abnormality in the production of transmitters since the brain’s functions. The paper has also discussed the role played by the antidepressant drugs in trying to stabilize the levels of neurotransmitters, thus reducing depression. The receptor theory may seem different from the other discussed methods since it claims that receptors and not neurotransmitters handle any mood control. Depression, when not treated can damage the brain, leading to mental health or change the brain structure as discussed in the paper. It is important to ensure that as a depression patient, a person should seek antidepressants, as failure to do so will affect even his physicality. In conclusion, the paper has illustrated that depression due to an imbalance of one or more biogenic amines and it can change the brain structure. References Chang, E. C. (2012). Handbook of adult psychopathology in Asians: Theory, diagnosis, and treatment. Oxford: Oxford University Press. Farooqui, A. A. (2010). Neurochemical aspects of neurotraumatic and neurodegenerative diseases. New York: Springer. McLeod, S. A. (2015). Biological Psychology. Retrieved from www.simplypsychology.org/biological-psychology.html Townsend, M. (2014). Psychiatric Mental Health Nursing: Concepts of Care in Evidence-Based Practice. Philadelphia: F. A. Davis Company. Read More