Disciplinary fragmentation and nosological and semantic controversies have obscured the impressive advances made in the area of depressive disorders during the past decade. This article is an attempt to translate data derived from psychodynamic, sociobehavioral, and neurobiologic research into a clinically meaningful framework. We review ten models of depression with special emphasis on newer models supported by empirical and experimental studies, and present a new model, which incorporates and synthesizes findings from different schools. Depressive illness is conceptualized as the feedback interaction of three sets of variables at chemical, experiential, and behavioral levels with the diencephalon serving as the field of action.

https://jamanetwork.com/journals/PSYCH/articlepdf/491325/archpsyc_32_3_001.pdf

Overview of recent research in depression. Integration of ten conceptual models into a comprehensive clinical frame.

Aversive experiences have been thought to provoke or exacerbate clinical depression. The present review provides a brief survey of the stress-depression literature and suggests that the effects of stressful experiences on affective state may be related to depletion of several neurotransmitters, including norepinephrine, dopamine, and serotonin. A major element in determining the neurochemical changes is the organism's ability to cope with the aversive stimuli through behavioral means. Aversive experiences give rise to behavioral attempts to cope with the stressor, coupled with increased utilization and synthesis of brain amines to contend with environmental demands. When behavioral coping is possible, neurochemical systems are not overly taxed, and behavioral pathology will not ensue. However, when there can be no behavioral control over the stressful stimuli, or when the aversive experience is perceived as uncontrollable, increased emphasis is placed on coping through endogenous neurochemical mechanisms. Amine utilization increases appreciably and may exceed synthesis, resulting in a net reduction of amine stores, which in turn promotes or exacerbates affective disorder. The processes governing the depletions may be subject to sensitization or conditioning, such that exposure to traumatic experiences may have long-term repercussions when the organism subsequently encounters related stressful stimuli. With continued uncontrollable stimulation, adaptation occurs in the form of increased activity of synthetic enzymes, and levels of amines approach basal values. It is suggested that either the initial amine depletion provoked by aversive experiences or a dysfunction of the adaptive processes, resulting in persistent amine depletion, contributes to behavioral depression. Aside from the contribution of behavioral coping, several organismic, experiential, and environmental variables will influence the effects of aversive experiences on neurochemical activity, and may thus influence vulnerability to depression.

Depression: The predisposing influence of stress

https://psycnet.apa.org/journals/bul/99/1/36.pdf

Conceptualization and measurement of human disorder in life stress research: the problem of chronic disturbance.

• Recent prospective studies suggest that thyroid state plays a role in affective disorders. A lack of thyroid hormones can lower the threshold for depression; an excess can contribute to a state of tense dysphoria. Thyroid function in some persons also appears to influence the course of affective disorders. Adequate mobilization of thyroid hormones favors recovery from depression; excess mobilization increases the risk of mania in vulnerable individuals. Although other mechanisms may be involved, evidence suggests that the modulation by thyroid hormones of the β-adrenergic receptor response to catecholamines may contribute to these effects. Norepinephrine stimulates such receptors; thyroid hormones increase their ability to receive stimulation. The plausibility of such interactions between catecholamines and thyroid hormones occurring in the CNS is strengthened by their common origin in the amino acid tyrosine and by their synergism in many metabolic processes.

https://jamanetwork.com/HttpHandlers/ArticlePdfHandler.ashx?journal=PSYCH&articleId=492471&pdfFileName=archpsyc_38_1_012.pdf

A Hypothesis of Thyroid-Catecholamine-Receptor Interaction: Its Relevance to Affective Illness

Learned helplessness in the perspective of the depressive disorders: conceptual and definitional issues.

An attempt is made to provide a cohesive conceptual frame upon which may be placed the recent advances in our understanding of the psychobiology of the affective disorders. Major literature in the ...

Anselm Parlatore

Papers

Melancholia, a Model in Madness: A Discussion of Recent Psychobiologic Research into Depressive Illness