Abstract
Article AbstractAlthough the monoaminehypothesis of depressionproposes that depressionis due to a deficiency inmonoaminergic neurotransmission,no deficiencies in the levels or receptorsfor serotonin, dopamine, and/ornorepinephrine have been consistentlyreported. Currently, the evolvingmonoamine hypothesis considersthe possibility that depression may belinked to a deficiency in signal transductionfrom the monoamine neurotransmitterto its postsynaptic neuronin the presence of normal amounts ofneurotransmitter and receptor. Such adeficiency in the molecular eventsthat cascade from receptor occupancyby neurotransmitter to transcription ofgenes could lead to a deficient responseof target neurons to neurotransmissionand thus, depression.
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