Peripheral Blood Cell Biological Markers in Depression

The classical monoamine hypotheses of depressive illness have postulated a deficiency of norepinephrine and/or serotonin at functionally important receptors in the central nervous system (CNS).1,2 An alternative “receptor hypothesis” would explain reduced transmission by a deficiency in signal amplification by the receptor complex. This focus on the receptor gained impetus from studies showing that virtually all effective somatic antidepressant treatment modalities shared the common effect of down-regulation and/or desensitization of β-adrenergic receptor complexes.3,4 Moreover, a significant number of antidepressants down-regulate 5- HT2 (serotonin; 5-hydroxytryptamine) receptors, although, in contrast, electroconvulsive shock up-regulates 5-HT2 receptors.4,5