PubMed · 8569585
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S Heinzl. 1995. [Depressing data on depression].. https://pubmed.ncbi.nlm.nih.gov/8569585/
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The development and configuration of several neural networks is dependent on the actions of serotonin (5-HT) acting through multiple hetero- and autoreceptor subtypes. During early brain development 5-HT modulates morphogenetic activities, such as neural differentiation, axon outgrowth, and synaptic modeling. In the adult brain, midbrain raphe serotonergic neurons project to a variety of brain regions and modulate a wide range of physiological functions. Several lines of evidence indicate that genetically determined variability in serotonergic gene expression, as it has been documented for the 5-HT transporter, influences temperamental traits and may lead to psychopathological conditions with increased anxiety, depression, and aggression. Investigation of the regulation of serotonergic gene transcription and its impact on neuronal development, synaptic plasticity, and neurogenesis spur interest to identify serotonergic gene-related molecular factors underlying disease states and to develop more effective antidepressant treatment strategies. Gene targeting strategies have increasingly been integrated into investigations of brain function and along with the fading dogma of a limited capacity of neurons for regeneration and reproducibility, it is realized that gene transfer techniques using efficient viral vectors in conjunction with neuron-selective transcriptional control systems may also be applicable to complex disorders of the brain. Given the fact that the 5-HT system continues to be an important target for drug development and production, novel strategies aiming toward the modification of 5-HT function at the level of gene expression are likely to be exploited by enterprises participating actively in the introduction of alternative therapeutic approaches.
Clinical and preclinical studies have gathered substantial evidence that alterations of the stress hormone system play a major, causal role in the development of depression. In this review article, a summary of studies sustaining that view is given and data are presented which demonstrate that depression is associated with an impairment of corticosteroid receptor function that gives rise to an excessive release of neurohormones to which a number of signs and symptoms characteristic of depression can be attributed. The studies referred to in the following unanimously support the concept of an antidepressant mechanism of action that exerts its effects beyond the cell membrane receptors of biogenic amines and particularly includes the improvement of corticosteroid receptor function. When activated by ligands, corticosteroid receptors act as transcription factors in correspondence with numerous other transcription factors already known to be activated by antidepressants. Furthermore, the potential of drugs that interfere more directly with stress hormone regulation, such as corticosteroid receptor antagonists and corticotropin-releasing hormone receptor antagonists, is discussed.
Recent advances in our understanding of both short- and long-term therapeutic interventions for depressive disorders have necessitated greater precision in defining appropriate therapeutic interventions. While these remarkable changes in treatment have been based on the introduction of newer antidepressant agents, the advances have occurred because of more systematic clinical trials and a greater sophistication in defining diagnostic and treatment response criteria. This paper reviews key findings in recurrent depression with respect to long-term treatment. Particular attention is paid to the combination treatment of psychotherapy and antidepressant drugs.