monoamine hypothesis

monoamine hypothesis

the classical theory of the neurochemical basis of depression linking it to a deficiency of at least one of three monoamine neurotransmitters: norepinephrine, serotonin, or dopamine.

mon·o·am·ine hy·po·the·sis

(mon'ō-ă-mēn' hī-poth'ĕ-sis)
The classical theory of the neurochemical basis of depression linking it to a deficiency of at least one of three monoamine neurotransmitters, norepinephrine, serotonin, or dopamine.
References in periodicals archive ?
The myth of reserpine-induced depression: role in the historical development of the monoamine hypothesis.
The monoamine hypothesis of depression postulates that symptoms originate from underactivity of monoamines, such as serotonin, norepinephrine, and dopamine, in the brain.
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.
1In the 1950s and 60s with the development of anti-depressant medications, the monoamine hypothesis and serotonin hypothesis came to dominate psychiatric research.
More than 50 years ago, researchers postulated a biological cause of depression called the monoamine hypothesis.
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.
Current pharmacotherapy is based on the monoamine hypothesis, which holds that depression is the result of depressed levels of certain substances--classified as monoamines--in the brain.
These problems focus on questions of the causal efficacy of placebos and drugs; ad hoc versus ceteris paribus explanations in biomedicine and psychology; and the falsifiability of the monoamine hypothesis.
IV ketamine therapy for severe de-pression is a dual paradigm shift: 1) it uses the IV route and 2) it modulates the glutamate ion-channel receptor NMD A--a major departure from the 50-year-old monoamine hypothesis of depression, in which a deficit of serotonin and/or norepinephrine was proposed.
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.