Table of Contents
What are the limitations of the monoamine theory of depression?
One of the drawbacks of the monoamine theory is that amine levels rise with antidepressant use instantly but maximum positive effects are not observed for several weeks with most antidepressants. To understand this delay in antidepressant effect, the time needed to synthesize neurotrophic factors has been suggested.
What supports the monoamine hypothesis of depression?
Serotonin has a role in some forms of depression Further support for this hypothesis comes from repeated findings of precipitation of depression during serotonin depletion in vulnerable individuals, as described above.
What is the monoamine deficiency theory of depression?
Abstract. The monoamine hypothesis of depression predicts that the underlying pathophysiologic basis of depression is a depletion in the levels of serotonin, norepinephrine, and/or dopamine in the central nervous system.
What is one reason why most researchers think the monoamine hypothesis is too simple?
However, the hypothesis was soon criticized because it was evident that increased availability of monoamines, due to inhibition of reuptake or metabolism, developed in a matter of hours, could not be the direct, mechanism of the therapeutic effect, which develops only after several weeks.
Why is the monoamine hypothesis not true?
The monoamine hypothesis, in failing to accurately explain the etiology of chronic neuronal electrical flow dysfunction in the endogenous state, is reduced to no more than a historical footnote.
What is a major problem with the treatment of depression by the administration of MAO inhibitors?
Rarely, an MAOI can cause dangerously high levels of serotonin, known as serotonin syndrome. It most often occurs when two medications that raise serotonin are combined. These include, for example, other antidepressants, certain pain or headache medications, and the herbal supplement St. John’s wort.
Which two monoamine neurotransmitters are most often associated with depression?
Multiple studies have implicated the monoamine neurotransmitters 5-hydroxytryptamine (5-HT or serotonin), dopamine (DA), and norepinephrine (NE) as the primary contributors to MDD etiology.
When was the monoamine hypothesis of depression?
In the 1950s, the amine hypothesis of depression was proposed after it was observed that patients treated for hypertension with reserpine developed depression [1].
What are the studies supporting the monoamine hypothesis?
Other evidence supporting the monoamine hypothesis comes from post-mortem studies of the brains of depressed people who unfortunately committed suicide. Some studies have found abnormally high numbers of serotonin receptors in the prefrontal cortex in suicide cases (Stanley and Mann, 1983; Yates et al., 1990).
What is the main theory of depression?
The diathesis-stress model, which is central to an understanding of depression, considers depression to be triggered by a combination of negative or stressful life event(s) (e.g. loss of an important source of love, security, identity or self-worth; death of a loved one, breakdown of a relationship or a significant …
Do depressed people have high levels of monoamines?
Their levels are lower in those who are depressed.
What is the major reason that monoamine oxidase inhibitors are rarely used in clinical practice today?
These are generally less utilized in current clinical practice due to their poor side-effect profile and potentially dangerous interactions with other drugs and foods, the latter reflecting the cheese, or tyramine, effect.
What is the monoamine hypothesis for anxiety?
The hypothesis proposes that the underlying neurobiological basis of anxiety and depression rests on the depletion of levels of key monoamine neurotransmitters: serotonin, noradrenaline (termed ‘norepinephrine’ in the US) and/or dopamine within the brain.
What are the dangers with monoamine oxidase inhibitors?
MAOIs can potentially cause drug-to-drug interactions, drug-food interaction, and overdoses, of which the patient should be aware. [9] For example, patients should not be mixing MAOIs with other antidepressants like selective serotonin reuptake inhibitors (SSRIs).
What is the bioamine theory of depression?
It has generally been assumed that these tricyclics alleviate depression by influencing the neurotransmitters (NA, 5-HT) at crucial receptor sites in the brain. Thus, the biogenic amine hypothesis of depression postulates that depression is due to a reduced functional activity of one or more brain amines.