Abstract
Deficiencies in the activity of specific pathways for serotonin (5-HT, 5-hydroxytryptamine), and norepinephrine (NE) have long been hypothesized to account for the symptoms of major depressive disorder (MDD). More than 30 years ago, it was noted that pharmacological agents that enhance the availability of the monoamine neurotransmitters serotonin, norepinephrine, and dopamine, produced a clinically meaningful improvement in mood in patients suffering from MDD. This clinical observation led to the development of the so-called 'monoamine hypothesis' of depression, which proposed that functional disruptions in these neurotransmitter systems mediate the behavioural and physiological symptoms (e.g. painful physical symptoms) of depression and related conditions. The pharmacotherapy of MDD has relied principally on the development of agents that alter or increase the functional activity of these classical neurotransmitter systems [1].
Highlights
en/p1I7n4te4r-n8a5t9ioXn-a5l-S1o-cfiueltl.ypdofn">Bhrearine.Burional Congress on Brain and Behaviour Meeting abstracts – A single PDF containing all abstracts in this Supplement is available
Adverse events resulting from the use of such drugs are frequently reported by patients as a reason for stopping treatment
Recent clinical evidence has accumulated that the selective enhancement of both 5-HT and NE systems provide a more robust clinical effect, e.g., in terms of higher remission rates [1]
Summary
en/p1I7n4te4r-n8a5t9ioXn-a5l-S1o-cfiueltl.ypdofn">Bhrearine.Burional Congress on Brain and Behaviour Meeting abstracts – A single PDF containing all abstracts in this Supplement is available
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