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. 2002 Mar;4(1):7-20.
doi: 10.31887/DCNS.2002.4.1/bbondy.

Pathophysiology of depression and mechanisms of treatment

Bondy Brigitta  1
Affiliations

Pathophysiology of depression and mechanisms of treatment

Bondy Brigitta. Dialogues Clin Neurosci. 2002 Mar.

Abstract
in English, Spanish, French

Major depression is a serious disorder of enormous sociological and clinical relevance. The discovery of antidepressant drugs in the 1950s led to the first biochemical hypothesis of depression, which suggested that an impairment in central monoaminergic function was the major lesion underlying the disorder. Basic research in all fields of neuroscience (including genetics) and the discovery of new antidepressant drugs have revolutionized our understanding of the mechanisms underlying depression and drug action. There is no doubt that the monoaminergic system is one of the cornerstones of these mechanisms, but multiple interactions with other brain systems and the regulation of central nervous system function must also be taken into account In spite of all the progress achieved so far, we must be aware that many open questions remain to be resolved in the future.

La depresión mayor es un trasiorno severo, de enorme importancia clínica y sociológica. El descubrimiento de los fármacos antidepresivos en ios años 1950 condujo a la primera hipótesis bioquimica de la depresión, la cual sugería que la principal lesión a la base de este trastorno era un deterioro de la función monoaminérgica central. La investigación básica en todos los campos de las neurociencias (incluyendo la genética) y el descubrimienio de nuevos fármacos antidepresivos han revolucionado nuestra comprensián acerca de los mécanismes fundamentales de la depresión y de la acción de las drogas. No hay dudas que el sistema monoaminérgico es una de las piedras angulares, pero también hay que tomar en cuenta las múltiples interacciones con otros sistemas cérébrales y la regulación de la función del sistema nervioso central. A pesar de todos los progresos alcanzados hasta la fecha, debemos estar conscientes de que existen muchas preguntas que deben ser resueltas en el futuro.

La dépression sévère est une maladie grave dont l'impact sociologique et clinique est immense. La découverte des antidépresseurs dans les années 50 a débouché sur la première hypothèse biochimique concernant la dépression, selon laquelle un déficit de la fonction monoaminergique centrale était l'anomalie principale sous-jacente à la maladie. La recherche fondamentale dans tous les domaines de la neuroscience (y compris génétique) et la découverte de nouveaux antidépresseurs ont bouleversé notre compréhension des mécanismes de la dépression et de son traitement Si le système monoaminergique est sans conteste l'une des pierres angulaires de ces mécanismes, les multiples interactions existant avec d'autres systèmes cérébraux et la régulation du système nerveux central doivent également être prises en compte. En dépit des nombreux progrès accomplis jusqu'à maintenant, de nombreuses questions demeurent toujours sans réponse.

Keywords: depression; genetics; monoamine; neurobiology; norepinephrine; serotonin; treatment.

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Figures

Figure 1.
Figure 1.. Schematic representation of a synapse and the steps of chemical transmission. Precursors are transported from blood into the brain (A), converted into transmitters via enzymatic processes, and stored in synaptic vesicles (B). The transmitters are released into the synaptic cleft (C), where they either react with presynaptic autoreceptors to regulate synthesis and release, or with postsynaptic receptors to induce the events of the downstream signal transduction cascade (D). MAO, monoamine oxidase.
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References

    1. American Psychiatrie Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed. Washington, DC: American Psychiatric Association; 1994.
    1. Garside RF., Kay DW., Wilson IC., Deaton ID., Roth M. Depressive syndromes and the classification of patients. Psychol Med. 1971;1:333–338. - PubMed
    1. World Health Organization. The ICD-10 Classification of Mental and Behavioral Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva, Switzerland: World Health Organization; 1992.
    1. Katz MM., Secunda SK., Hirschfeld RM., Koslow SH. NIMH clinical research branch collaborative program on the psychobiology of depression. Arch Gen Psychiatry. 1979;36:765–771. - PubMed
    1. Gurland B. Aims, organization, and initial studies of the Cross-National Project. IntJ Aging Hum Dev. 1976;7:283–293. - PubMed

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