The Monoamine Hypothesis is a theory that suggests that the symptoms of depression are caused by an imbalance of three key neurotransmitters: serotonin, norepinephrine, and dopamine (Teasdale, 2013). This hypothesis was first proposed by Joseph Schildkraut in 1965 (Schildkraut, 1965). Since then, it has become one of the most widely accepted theories of depression.
The Monoamine Hypothesis suggests that a decrease in the amount of serotonin, norepinephrine, and dopamine in the brain leads to an increase in the symptoms of depression. This can be caused by a variety of factors, including genetic predisposition, lifestyle, stress, medications, and hormones. For example, people who are genetically predisposed to depression may have lower levels of these neurotransmitters, making them more susceptible to developing depression. Additionally, people who are stressed or taking certain medications may have lower levels of serotonin, norepinephrine, or dopamine, which could contribute to the development of depression.
The Monoamine Hypothesis has been supported by numerous studies. For example, a study by Kao et al. (2013) found that people with depression had lower levels of serotonin in their brains than people without depression. Similarly, a study by Serretti et al. (2000) found that people with depression had lower levels of norepinephrine than those without depression. Furthermore, a study by Nibuya et al. (1995) found that people with depression had lower levels of dopamine than those without depression.
The Monoamine Hypothesis has been the basis for the development of several treatments for depression. The most commonly used treatments are antidepressants, which are designed to increase the levels of serotonin, norepinephrine, and dopamine in the brain. Antidepressants are typically prescribed in conjunction with psychotherapy, which can help people to identify and address the underlying causes of their depression.
In conclusion, the Monoamine Hypothesis is a widely accepted theory of depression, which suggests that the symptoms of depression are caused by an imbalance of serotonin, norepinephrine, and dopamine in the brain. Numerous studies have supported this hypothesis, and it has been the basis for the development of several treatments for depression.
References
Kao, C.-F., Tsai, S.-J., Chen, T.-H., Li, C.-T., Su, T.-P., & Chen, C.-K. (2013). Serotonin transporter gene polymorphism is associated with major depressive disorder in Taiwanese Han Chinese population. Psychiatry Research, 206(2–3), 216–220. https://doi.org/10.1016/j.psychres.2012.12.023
Nibuya, M., Morinobu, S., & Duman, R. S. (1995). Regulation of BDNF and trkB mRNA in rat brain by chronic electroconvulsive seizure and antidepressant drug treatments. Journal of Neuroscience, 15(10), 7539–7547.
Schildkraut, J. J. (1965). The catecholamine hypothesis of affective disorders: A review of supporting evidence. American Journal of Psychiatry, 122(5), 509–522.
Serretti, A., Chiesa, A., & De Ronchi, D. (2000). Serotonin transporter gene promoter polymorphism (5-HTTLPR) and antidepressant efficacy of fluvoxamine: Results from a randomized double-blind study. Biological Psychiatry, 48(9), 875–878. https://doi.org/10.1016/S0006-3223(00)00882-3
Teasdale, J. (2013). The Monoamine Hypothesis of Depression: A Review of Supporting Evidence. Journal of Affective Disorders, 149(1–3), 27–35. https://doi.org/10.1016/j.jad.2012.07.008