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Deficiency of Neurotransmitters and Its Relationship with Major Depressive Disorder

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Deficiency of Neurotransmitters and Its Relationship with Major Depressive Disorder

Major depressive disorder (MDD) has been identified as a major health problem

globally. It is estimated that 3.8% of the global population suffers from depression with men

showing higher proportions (Drevets, 2022). Despite these trends, the triggers of MDD still

remain relatively unclear with researchers associating the disorder with several factors. The

deficiency of neurotransmitters is one of the most acclaimed reasons (Gong et al., 2017; Nutt,

2008). The shortage of neurotransmitters causes MDD through three main process, namely

disruption of reward processing, reduced neuroplasticity, and disrupted mood regulation.

One of the most prevalent mental diseases, depression is also one of the primary

causes of disability across the globe. Regardless of decades of study, the understanding of the

neuropathological pathways underlying depression is still limited. Depression is a complex

mental condition with a variety of symptoms that may have separate causes. Anhedonia is

being recognized as a hallmark of depression and is linked to a higher suicide risk and less

successful therapy (Ng et al., 2019). As a kind of a spectrum of disorders in the reward

circuit, anhedonia is characterized by a lack of enthusiasm or delight in things that were

formerly pleasant. The neurobiology of anhedonia has been linked to reward system

malfunction in many studies (Ng et al., 2019; Drevets, 2022). Several sorts of reward-related

processing abnormalities, including reward response bias, reduced reward learning capacity,

and greater risk aversion, have been seen in depressed individuals, according to behavioral

research (Argyropoulos & Nutt, 2013; Costello et al., 2022). Hence, disrupted reward system

is likely to lead to MDD.

The word "neuroplasticity" is used to describe a range of changes that may be

triggered in the brain and spinal cord in response to external influences (Brüchle et al., 2021;

Rădulescu et al., 2021). The brain has the ability to change its shape and reorganize its

connections by either reinforcing or inhibiting synaptic communication. Some

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antidepressants aid neuroplasticity processes by mending broken neural circuits, enhancing

synapses in targeted regions of the brain, or restoring normal glutamatergic levels (Brüchle et

al., 2021; Rădulescu et al., 2021). Furthermore, the muscle-coated fibers and the pyramidal

neurons of the hippocampus may provide insight into the organic alterations at the synapses.

As a result, the amygdala, which serves an essential part in processing emotions and social

development, the hippocampus, which contributes to learning and memory, and the prefrontal

cortex, which is concerned with attention, concentration, learning, and memory, all have

challenges functioning normally in people with major depressive disorder (Yun, & Kim,

2022). Thus, the reduced amount of neurotransmitters leads to neuroplasticity, which results

in MDD.

Imbalances in neurotransmitters have been linked to major depressive disorder

(MDD) via a variety of pathways. Liu et al., 2018 report that serotonin and norepinephrine

levels in the brains of people with MDD are lower than in healthy people, suggesting a

probable shortage in these neurotransmitters. Both low serotonin and norepinephrine levels

have been related to elevated negative affect and reduced positive affect, respectively as

revealed by Joormann & Gotlib, (2010). Dopamine, in addition to serotonin and

norepinephrine, has been shown to have a role in maintaining emotional stability. Joormann

& Vanderlind (2014) posit that dopamine activity in the brain's reward pathways is decreased

in people with MDD, which may contribute to the anhedonia or lack of pleasure often seen in

people with the illness. Consequently, MDD may develop.

In conclusion, neurotransmitters play an important role in the spread of MDD. The

reduction in neurotransmitters interferes with the physiological functioning of the mental

faculties through three main processes. Impaired mood regulation, reduced neuroplasticity,

and disrupted reward systems all lead to depressive symptoms in affected individuals. Several

studies support this thesis as shown in the literature review.

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References

Argyropoulos, S. V., & Nutt, D. J. (2013). Anhedonia revisited: is there a role for dopamine-

targeting drugs for depression? Journal of psychopharmacology, 27(10), 869-877.

https://doi.org/10.1177/0269881113494104

Brüchle, W., Schwarzer, C., Berns, C., Schneefeld, J., Koester, D., Schack, T., &

Rosenkranz, K. (2021). Physical activity reduces clinical symptoms and restores

neuroplasticity in major depression. Frontiers in Psychiatry, 12, 660642.

https://doi.org/10.3389/fpsyt.2021.660642

Costello, H., Berry, A. J., Reeves, S., Weil, R. S., Joyce, E. M., Howard, R., & Roiser, J. P.

(2022). Disrupted reward processing in Parkinson’s disease and its relationship with

dopamine state and neuropsychiatric syndromes: a systematic review and meta-

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Gong, L., Yin, Y., He, C., Ye, Q., Bai, F., Yuan, Y., & Zhang, Z. (2017). Disrupted reward

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Jiang, Y., Zou, D., Li, Y., Gu, S., Dong, J., Ma, X., & Huang, J. H. (2022). Monoamine

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Joormann, J., & Vanderlind, W. M. (2014). Emotion Regulation in Depression: The Role of

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