Mood, amine hypothesis

As outlined previously, initial biological hypotheses of mood disorders were derived from the pharmacological actions of antidepressant drugs, which increase synaptic concentrations of noradrenaline (NA] and/or serotonin. Consequently, the biogenic amine hypothesis was formulated, but it lacks consistent proof that NA and/or serotonin release is indeed diminished. This failure is in part a result of the limited access to relevant brain areas. Measurements of NA and serotonin and their metabolites in blood, urine, and CSF... 

Keywords Major depressive disorder Biopolar disorder Schizophrenia Mood disorders Biogenic amine hypothesis Learned helplessness Antidepressant drugs Mood stabilizers Dopamine hypothesis Antipsychotic drugs... 

Amine hypothesis of mood The hypothesis that major depressive disorders result from a functional deficiency of norepinephrine or serotonin at synapses in the central nervous system... 

The amine hypothesis of mood postulates that brain amines, particularly norepinephrine (NE) and serotonin (5-HT), are neurotransmitters in pathways that function in the expression of mood. According to the amine hypothesis, a functional decrease in the activity of such amines would result in depression a functional increase of activity would result in mood elevation. Difficulties with this hypothesis include the facts that (1) antidepressant drugs cause changes in amine activity within hours, but weeks may be required for them to achieve clinical effects (2) most antidepressants ultimately cause a down-regulation of amine receptors and (3) at least one antidepressant, bupropion, has minimal effects on brain NE or 5-HT. 

Several mechanisms exist to explain the etiology of affective disorders all based on the hypothesis that certain levels of amine neurotransmitters (e.g., norepinephrine - NE, serotonin - 5-HT) and receptor sensitivity are necessary for normal mood. There is ample evidence that depression occms if receptors are insensitive or if amine synthesis, storage or... 

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