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Monoamines are a group of organic compounds containing only one amino group.

Several mood disorders are explained as due to either an excess or deficiency of monoamines. When a cell needs to transport a monoamine in or out of a cell, they use a class of proteins called monoamine transporters.

The pathophysiology and effects of antidepressants in the brain are still poorly understood. While it is generally accepted that increasing the levels of monoamine in the brain is an effective way to alleviate depression, the precise neurobiological mechanisms are unclear. The evidence that monoamine function is impaired in individuals with depression is largely indirect. However, the neurotransmitter depletion model allows a more direct investigation of the role of the monoamines.

Rasagiline [N-propargyl-1R(+)-aminoindan; TVP1012] is a potent irreversible monoamine oxidase (MAO) inhibitor with selectivity for type B of the enzyme, which is being developed for treatment of Parkinson's disease.

Monoaminergic pathways are highly responsive to aversive stimuli and play a crucial role in the control of affect, cognition, endocrine secretion, chronobiotic rhythms, appetite, and motor function, all of which are profoundly disrupted in depressive states. Accordingly, a perturbation of monoaminergic transmission is implicated in the aetiology of depressive disorders, and all clinically available antidepressants increase corticolimbic availability of monoamines. However, their limited efficacy, delayed onset of action, and undesirable side effects underlie ongoing efforts to identify improved therapeutic agents. Sequencing the human genome has raised the hope not only of better symptomatic control of depression, but even of the prevention or cure of depressive states. In the pursuit of these goals, there is currently a tendency to focus on selective ligands of novel nonmonoaminergic targets. It is important to continue the creative exploration of clinically validated and innovative monoaminergic strategies within a multitarget framework. In this light, drugs combining monoaminergic and nonmonoaminergic mechanisms of action may be of particular interest.

Monoamines and depression

There is good evidence that unmedicated depressed patients have abnormalities in various aspects of monoamine function. However, these abnormalities vary in extent from case to case, and the changes are not large and are not sufficiently sensitive to be diagnostic.

The most convincing studies that show a key role for monoamines in the pathophysiology of depression are the 5-HT and catecholamine depletion paradigms. It is now established that in vulnerable individuals, lowering of 5-HT and noradrenaline and dopamine function is sufficient to cause clinical depression. Two major question emerge from this work:

  1. What mechanism produce low monoamine function in depressed patients?
  2. What are the other factors that make those at risk of depression psychologically vulnerable to manipulations of monoamines function?

Both these questions might be addressed by improving our understanding of the actions of monoamines at a cellular level.

The cause of depression therefore appears to be more complex than simply a reduction in levels of monoamine or diminished function in these systems. The pathophysiology of depression may relate to dysfunction in brain areas modulated by monoamine systems. Antidepressant drugs may mediate their effects by causing adaptive changes in neurones localized in these brain areas.

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