Serotonin Hypothesis of Depression Biologyâ€Myassignmenthelp.Com

Question: Explain on Serotonin Hypothesis of Depression Biology? Answer: Introduction Serotonin or 5-hydroxytryptophan (5-HT) is a neurotransmitter found in the central nervous system of humans, and it helps in the transmission of impulses. It triggers the release of chemical into the brain hence causing migraine pain. However, the serotonin theory of depression holds that increased level of mania or depression is linked to low serotonergic activities (Asberg et al., 1976). For the last two decades, studies on platelets and cerebrospinal fluid of the depressed patients showed serotonergic abnormalities. Over the last decade, research on 5-HT dysfunction in the mental illnesses has used advances in molecular biology and neuroimaging to classify mental disorders. This essay will explore the role of serotonin in the etiology of depression. Evidence supporting or opposing the role 5-HT in causing depression will be discussed in detail Evidence For and Against the Serotonin Hypothesis of Depression One approach that has been used to investigate the connection between serotonin and depression is the receptor binding studies (Drevets et al., 1999). The studies show that depression is associated with a reduction in 5-HT uptake sites as well as control in some categories of the serotonin receptors. However, the challenge is to incorporate the separate findings into a hypothesis. One theory holds that alterations in the serotonin receptors would represent an initiating factor relative to the compensator response. This means that increases in the 5-HT transmission would mediate depressive symptoms because of the signals in the postsynaptic regions. As a result, levels of the neurotransmitter plus their metabolite might be expected to go down. A latter model postulates that increase in the 5-HT activities would mediate depression via alterations in the neurotransmitter receptors (Healy, 2015) In another study, depression is caused by administration of serotonin plus defined regarding the degree of animal activities. In the depressive form, certain uptake blockers of 5-HT were found to increase the power of depressive symptoms significantly. Accounting to Neuemeister (2002) the increase in depressive behaviors was involved with the growth of serotonin metabolite in the brain. In contrast, 5-HT induced depressions were abolished by Mianserin among other antidepressants that put their effect through blocking 5-HT postsynaptically. In simple terms, the data implies that depression might be mediated through postsynaptic as well as induced via abundant transmission of neurotransmitter at the synapse. All in all, theres strong evident that suggests depression is linked with low levels of 5-HT uptake sites plus an increase in classes of neurotransmitter receptors. However, it's yet to be known whether receptor alterations represents the primary or secondary effects of low 5-HT content Animal studies show that 5-HT receptors found on the serotonin cells in the midbrain plays a vital role in the release of 5-HT in a region in the path physiology of major depressive disorder. However, activation of neurotransmitter receptors in the brain hinders the release of serotonin neurons as well as lowers firing of the 5-HT in the prefrontal cortex (Shopsin and Frank, 1984). The chronic treatment with medications including monoamine oxidize inhibitors desensitizes neurotransmitter receptors in the brain. The serotonin receptor inhibiting mechanism in the brain might be boosted in major depressive disorder as well as might be a target for desensitization by the antidepressant medications. On the other case, altered serotonergic mechanisms in the brain might play a vital role in pathophysiology of major depressive disorder as well as suicide (Healy, 2015). Neuroimaging studies have also shown the alterations in the 5-HT transporter in depression. However, the presence of neurotransmitter in the brain is reported as in decline among adult with major depressive disorder plus increased in the midbrain in depressed teenagers and children. When compared with the healthy controls, the presence of 5-HT transporter is lowered in a Cephalon in the seasonal affective disorder as well as not changed in the striatum in major depressive disorder (Stockmeier, 2003). All in all, its hard to compare postmortem studies with imaging of 5-HT in a human brain. This is because neuroimaging studies examine living depressed subjects with less spatial resolution contrary to spatial resolutions in the post-mortem studies Conclusion Different studies of depression have used imaging and post-mortem techniques to investigate 5-HT receptors as well as serotonin transfer. However, alteration in the serotonin alone cannot fully accounting for the complex cause as well as treatment of Major Depressive disorders. Also, studies in the neither postmortem brain tissues show norepinephrine in major depressive disorder as well as suicide. Besides, monoamine transmitters, clinical studies also argue that neurokinin and amino butyric acid might also be involved in the cause as well as treatment of depression References Asberg, M., Thoren, P., Traskman, L., Bertilsson, L., Ringberger, V. (1976). " Serotonin depression"--a biochemical subgroup within the affective disorders?. Science, 191(4226), 478-480. Drevets, W. C., Frank, E., Price, J. C., Kupfer, D. J., Holt, D., Greer, P. J., ... Mathis, C. (1999). PET imaging of serotonin 1A receptor binding in depression. Biological psychiatry, 46(10), 1375-1387. Healy, D. (2015). Serotonin and depression. BMJ, 350, h1771. Neumeister, A. (2002). Tryptophan depletion, serotonin, and depression: where do we stand?. Psychopharmacology bulletin, 37(4), 99-115. Shopsin, B., Frank Feiner, N. (1984). Serotonin and depression. In Serotonin in Affective Disorders (pp. 1-11). Karger Publishers. Stockmeier, C. A. (2003). Involvement of serotonin in depression: evidence from postmortem and imaging studies of serotonin receptors and the serotonin transporter. Journal of psychiatric research, 37(5), 357-373.