The Symptoms, Neurobiology, and Current Pharmacological Treatment of Depression

Stephen E. To; Robert A. Zepf; Alisa G. Woods

J Neurosci Nurs. 2005;37(2):102-107. 

In This Article

Neurotransmitter Hypothesis of Depression

For many years, the prevailing hypothesis of depression has been that a deficit in monoamine neurotransmitters, notably norepinephrine and serotonin, underlies depression. The monoamines are named because of their synthesis from amino acid precursors—tryptophan for serotonin and tyrosine for norepinephrine, epinephrine, and dopamine. 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. Although current theories recognize that depleted monoamine neurotransmitters may be involved in the pathogenesis of depression, they also acknowledge that other factors may be involved.

Although existing antidepressant medications increase levels of monoamines in the brain, there is a delay between measured increases in monoamines and corrections in mood. Antidepressants may act on other neurotransmitters, such as acetylcholine and gamma-aminobutyric acid (GABA). The monoamines, serotonin and norepinephrine also influence and are influenced by other processes in the brain. The neurochemical basis of depression now is regarded as being more complex and not the result of any one specific deficit. For example, the function of the hypothalamic pituitary axis and the involvement of stress-related hormones are increasingly believed to play a role in the development of depression (Kandel, 2000).

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