Exam
Introduction
Generally, most patients with depression require specific antidepressant medications. These drugs play a critical role in relieving specific factors and influences contributing to depression among affected people. Although the pharmaceutical therapies have been effective and reliable in ensuring positive outcomes in improving conditions and issues among most patients with this depression, they in some cases work at the synaptic level. As a result, the impacts of these drugs can be seen after a while, wither within a matter of minutes to hours. Typically, such outcomes are mainly related to specific biological factors affecting how antidepressant drugs. This paper will therefore focus on biological factors affecting the general impact, performance, and role of antidepressants on patients. The focus will therefore be based on neurotransmitter-based explanations with a primary objective of understanding how such biological factors affect the psychological process of the brain, particularly in the case of depressions.
Depression is mainly related to an individual’s state of chemical imbalances. As a result, antidepressants work mainly by increasing monoaminergic neurotransmission to balance the state of chemical imbalance. Antidepressant drugs tend to be associated mainly with the induction of neuroplasticity in specific structures. These structures include the prefrontal cortex and, most importantly, the hippocampus. As a result, they tend to influence the stimulation processes on dendritic arborization, neurogenesis, and in some cases, gliogenesis and other new formations relate to synapse. In some cases, these changes play a critical role, particularly in underlying specific working mechanisms of responses related to these antidepressants. The main reason, in this case, is related to the fact that the time course of these antidepressant drugs in consideration to their action is affected as a result of a reverse in the effects related to neurophysiological stress. Besides, they, in some cases, provide an opportunity for relearning specific, desired, and healthier cognitions, behavioral expressions, and most importantly, healthy responses related to an individual’s emotions. As a result, the neuroplasticity of these drugs cannot be considered certain or complete in any way. One of the main reasons is related to the fact that it fails to explain why ECT, ketamine, and scopolamine tend to have significant effects on antidepressants. Consequently, the neuroplasticity hypothesis related to antidepressant actions tends to be more complete and, most importantly, plausible than antidepressant actions from earlier hypotheses (Andrade & Rao, 2010).
Neuroplasticity plays a critical role in influencing the ability of an individual’s neural system to become effective, particularly in adapting itself to both external and, most importantly, internal stimuli, thus ensuring positive outcomes in its ability to respond adaptively to possible stimuli. Generally, the neuroplasticity process tends to be complex. As a result, its underlying mechanisms have not been understood more effectively. Antidepressant drugs work mainly by improving neuroplasticity. The improvements are achieved through monoamine neurotransmitters stimulations related to receptors of the postsynaptic monoamine. Neuroplasticity of major depressive disorder, therefore, changes from the monoamine hypothesis with a focus on addressing specific issues related to the monoamine hypothesis. Receptors related to NMDA and, most importantly, potentiation of AMPA receptors play a major role in affecting the efficacy of antidepressants, particularly ketamine (Liu et al., 2017). Activation of the postsynaptic monoamine plays a critical role in the activation of the postsynaptic monoamine receptor. Besides, it also helps in the neuroplasticity path. However, this path has been proved to be much slower and weaker, particularly than direct working in consideration to receptors related to inotropic glutamate. Logically, ketamine tends to take a faster speed and, in most cases shorter route when it comes to the regulation of neuroplasticity. SSRIs, on the other hand, take slower speed and longer routes. These cases mean ketamine results in a fast response, while SSRIs will contribute to a delayed onset in the general regulation of neuroplasticity (Zhang et al. 2019).
Based on the postsynaptic effects of these drugs, particularly in long-term treatments, affected people may experience several days or months elapsing before the first effects of these drugs takes place. Generally, blockage in consideration to the uptake of neurotransmitters tends to occur in the brief time required to ensure the effectiveness of the body concentration of the drug. Most of these antidepressants tend to raise levels of catecholamine, particularly at postsynaptic receptor sites. The main reason is that they tend to inhibit reuptake and, most importantly, monoamine oxide degradation related to different biogenic amines. As a result, it contributes significantly to the desensitization of the presynaptic autoreceptor. In such situations, norepinephrine release tends to be increased (Richelson, 1990, September). Logically, hypothesis desensitization tends to assume that specific receptors related to catecholamine are supersensitive, particularly on people with depression. As a result, the primary role of antidepressant drugs is mainly to return them to normal levels that are required to ensure effectiveness and positive outcomes in consideration to their sensitivity.
Besides, the monoamine hypothesis related to depression tends to be attributed to specific symptoms related to major depressive disorders to imbalances of dopamine, serotonin, and most importantly, noradrenaline. These are mainly related to the brain’s limbic area. Although SSRIs have been improved and believed to work best, they, in some cases and some patients, fail to ensure effectiveness and positive outcomes in resolving depression. These drugs, therefore, may contribute to issues of some antidepressant drugs (Edinoff et al., 2021). Generally, the inconsistency, in this case, can be related to the current hypothesis that the rise in the cases of clozapine dosage and, in some cases, the addition of fluvoxamine. However, a combination of treatments, particularly fluvoxamine and clozapine, have been proved to be effective and reliable in ensuring effective treatment and an important option for most patients. As a result, the impacts of these biological factors continue to influence the general impacts and, most importantly, the efficacy of most antidepressant drugs.
Conclusion
Different antidepressant drugs have different effects on patients. Generally, these impacts and how they respond to solving specific issues and problems of any depressive disorder are affected by specific factors and problems contributing to the general response and impacts of the drugs. As a result, understanding the hypothesis of antidepressants and, most importantly, how they influence specific biological factors can help to ensure effectiveness and positive outcomes in understanding how the patients are affected and how these drugs help to influence and ensure improvements from these issues. The biological factor, in this case, limits effectiveness in the normal psychological process of the body, as a biological factor plays a critical role in affecting how these drugs work with a primary aim of improving conditions and issues affecting general conditions of patients. However, understanding these factors can help to make specific improvements and reliable responses that will ensure positive impacts on the health of patients.
References
Andrade, C., & Rao, N. S. K. (2010). How antidepressant drugs act: a primer on neuroplasticity as the eventual mediator of antidepressant efficacy. Indian journal of psychiatry, 52(4), 378.
Edinoff, A. N., Fort, J. M., Woo, J. J., Causey, C. D., Burroughs, C. R., Cornett, E. M., … & Kaye, A. D. (2021). Selective Serotonin Reuptake Inhibitors and Clozapine: Clinically Relevant Interactions and Considerations. Neurology International, 13(3), 445-463.
Liu, B., Liu, J., Wang, M., Zhang, Y., & Li, L. (2017). From serotonin to neuroplasticity: evolvement of theories for major depressive disorder. Frontiers in cellular neuroscience, 11, 305.
Richelson, E. (1990, September). Antidepressants and brain neurochemistry. In Mayo Clinic Proceedings (Vol. 65, No. 9, pp. 1227-1236). Elsevier.
Zhang, X., Yin, Y., Yue, L., & Gong, L. (2019). Selective serotonin reuptake inhibitors aggravate depression-associated dry eye via activating the NF-κB pathway. Investigative ophthalmology & visual science, 60(1), 407-419.
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