The monoamine hypothesis was first introduced during the 1950s and researchers found that the level of serotonin in the brain might be related to the etiology of mood disorders (Hirschfeld, 2000). Over more than three decades, lots of research tried to focus on how the change of the number of monoamine neurotransmitters in our brain might contribute to one of the well-known disorders – depression (Delgado, 2000; ). The main idea of the monoamine hypothesis is that depression is caused by a deficiency in the levels of monoamine neurotransmitters which are serotonin, norepinephrine and/or dopamine (Delgado, 2000; Hirschfeld, 2000). The idea was supported by the use of antidepressants. Reports, conducted by (Delgado, 2000; 1955,etc) showed that there is an improvement for patients to alleviate their depression symptoms after taking the antidepressants. In order to help patients who suffered from depression, scientists developed many different types of antidepressant agents which either inhibit the degradation of those three neurotransmitters or stop their action of reuptake by simply blocking it (Hirschfeld, 2000). First, depletion in the concentration of serotonin in the synaptic cleft would end up with major depressive disorder (MDD) on the basis of the monoamine theory. Delgado (2000a) mentioned that patients with depression showed a low level of 5- hydroxyindoleacetic acid (5-HIAA) which is a major serotonin metabolite. More important, there was a relatively small number of serotonin transporter sites in antidepressant-naïve patients compared to normal people and it was not found in other mood disorders like mania and panic disorder (2000a). Thus, many antidepressants were produced in increasing the level of serotonin such as tricyclic antidepressant and serotonin selective reuptake inhibitor. A tricyclic antidepressant (TCA) is one of the antidepressants in the early development of depression and has been used for many years in the depression treatment (Hirschfeld, 2000). One of the purposes is to inhibit the reuptake of serotonin so that the monoamines could get into the receptors to maximize the effect. However, there are a lot of undesirable side effects of TCAs because it blocks various neurotransmitter receptors. For example, patients were shown effects like constipation and drowsiness by blocking the acetylcholine receptors and histamine receptors (1998; Hirschfeld, 2000). Notably, it could be lethal in overdose. Another widely prescribed serotonergic antidepressant agent is a serotonin selective reuptake inhibitor (SSRI). It selectively targets the serotonin reuptakes unlike the TCAs, which affect many other receptor sites. The side effects of the drug can be significantly reduced but it still contains some unwanted effects like headache and nausea (Hirschfeld). In addition, one potential problem is that the SSRIs have been tested to be effective in other mental disorders such as …show more content…
Bupropion is an antidepressant drug that selectively inhibits the reuptake of norepinephrine and dopamine. Depressed patients who did not respond to the SSRI could use bupropion to improve their symptoms, but the side effects are also presented, especially seizures which are four times higher to occur in bupropion than other antidepressants (1998). Like serotonergic antidepressants, the article (1998) noted that bupropion has been shown to be effective in many other disorders such as attention deficit disorder. Therefore, it is linked to the same problem that the monoamine theory might not be the critical reason to cause depression.
The use of antidepressant agents address the concern that we need to consider thoughtfully on the relationship between monoamine depletion and depression. Not only the drugs were shown to be effective in other mental disorders, but also there are other problems which are the delay in the onset of the effect (Hirschfeld); no effect on most of the subjects in many studies (Kirsch); and the argument about the serotonin-transporter-linked polymorphic region (Lopez-Leon et al., 2005). Any one of these would challenge the credibility of the monoamine