The development, nearly 50 years ago, of the monoamine hypothesis of depression has been a driving force behind research and drug development in the decades since.
The two key neurotransmitters implicated in the monoamine hypothesis are noradrenaline and serotonin.
The monoamine hypothesis suggests that, in the brain of the depressed person, there is dysfunction in neurotransmission of serotonin and/or noradrenaline, and perhaps dopamine, due to any of the following:
Support for the monoamine hypothesis comes from observations that drugs designed to increase neurotransmitters in the brain relieve symptoms of depression.
This monoamine hypothesis originated in the 1950s with the observation that an antihypertensive medication called reserpine depletes the brain of norepinehrine, serotonin, and dopamine, causing depression.
Despite the replacement of the monoamine hypothesis of depression with a more comprehensive understanding of multiple influencing factors in the pathology of depression, it is clear that elevating monoamines does result in an elevation in mood in many depressed individuals.
The evolution of antidepressant therapy, spurred by the monoamine hypothesis of depression, has resulted in a large number of available pharmacotherapies to combat this prevalent health problem.
Currently, the favoured theory for depression is the monoamine hypothesis, which proposes that depression is primarily a consequence of decreased (or relatively decreased) noradrenaline (NA) and/or serotonin (5HT) neurotransmitter activity in the brain.
Antidepressant pharmacotherapy, for moderate to major depression, aims to increase the amount of serotonin and/or noradrenaline at post-synaptic receptor sites and this, in turn, improves mood and hence Lends support to the monoamine hypothesis of depression.