A team of scientists in the 1950s stumbled across the idea for this hypothesis during the trials for blood pressure medication, Reserpine, which reduces the release of norepinephrine and serotonin in the brain and was found to precipitate depression in some patients. Reserpine was also found to produce depressive symptoms in animals (Hirschfeld, 2000). It was found to inhibit vesicular monoamine transporters, and as a result, depleted brain monoamines, which provides evidence for the role of serotonin, norepinephrine and dopamine in depression (Kirshner, 1962; Shore, Pletscher, Tomich, Carlsson, Kuntzman , & Brodie, 1957; Shore, Silver, &Brodie 1955: Weiner, Cloutierm Bjur, &Pfeffer, 1972) This gave birth to the monoamine hypothesis.
In 1950s whilst treating patients with anti-tuberculosis medication Iponiazid, clinicians noticed side effects which included euphoria, psycho-stimulation, increased appetite and improved sleep. Further research by Loomer confirmed significant improvement in the symptoms of depression in 70% of the patients. So this became the first successful treatment for depression and is considered a MAO inhibitor.
According to the monoamine hypothesis, depression can be ascribed to deficiency in the monoamine neurotransmitters: serotonin, dopamine and noradrenaline, which affect mood. The studies into antidepressant medications have shown that drugs increasing the synaptic levels of monoamine transmitter serotonin, have alleviated the symptoms of depression. This indicated that serotonin plays a big part in depression and increasing levels of serotonin accidentally, alerted the scientists to study this neurotransmitter further, leading to the monoamine hypothesis.
The hypothesis suggests that deficit of certain neurotransmitters at the synapse is responsible for corresponding features of depression. In the late 1960, evidence emerged suggesting the importance of serotonin. A postmortem study revealed decreased concentrations of...