Neuropsychologists used a functional magnetic resonance imaging (fMRI) on depressed patients to see how differences in the brain activity when compared to normal people and the result showed that depressed patients have a decreased activity in dorso lateral pre-frontal cortex (DLPFC) but the activity of the amygdala, where is responsible to our emotional reactions such as sadness and happiness, was relatively increased (2007). It would then explain why patients who suffered from depression tend to have an emotional flooding.
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 …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
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 …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