How to critically analyze this? Major Depressive Disorder (MDD) is a leading cause of disability, with around 300 millio

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How to critically analyze this?
Major Depressive Disorder (MDD) is a leading cause ofdisability, with around 300 million people afflicted withdepression worldwide, according to the World Health Organization[1]. Symptoms of depression include heightened negative affect(negative moods, e.g., feeling nervous, scared, and guilt, etc.)and diminished positive affect (positive moods, e.g., feeling lessmotivated, loss of pleasure, harder to concentrate, etc.). Inaddition to causing personal distress, depression also plays alarge role in suicide attempts, with one-half of all suicideattempts linked to depression and nearly 20% lifetime suicide riskif left untreated [2]. Despite the large volume of studies devotedto depression research, our understanding of depression is stilllimited to this day, partially because depression is aheterogeneous disease that varies in symptomologies and underlyingpathophysiology [3, 4]. Because the fundamental etiology ofdepression is not clear, recreating a perfect animal depressionmodel that captures every and all aspects of the disease is nearlyimpossible. Nonetheless, psychologists proposed various animalmodels in the past decades in the hope to explain the formation ofsome core phenotypic characterizations that we see in humandepression patients [5, 6]. Central to the animal depressionmodels, some of the most widely used ones are the learnedhelplessness (LH) model, the chronic mild stress (CMS) model, theearly life stress model, and the social defeat model [5]. Thesemodels simulate different processes that may lead to thedevelopment of depression, and each paradigm produces a set ofbehavioral features in animals that resemble a depressed-like statein humans. Although the animal models vary in the extent to whichthey resemble human depressive states, a disease model is onlyconsidered a good model when it has good face validity, constructvalidity, and predictive validity [7, 8]; in other words, agood animal depression model should have the followingcharacteristics: (1) produce behavioral changes that aresimilar to those seen in human depression; (2) the changescan be objectively measured; (3) the changes can bereversed by treatments used to treat depression. An idealdepression model should recreate the complex, multidimensionalsymptom profiles of the human depression state. In this study, weaim to examine the learned helplessness depression model andanhedonia, a key symptom in depression.
The learned helplessness (LH) model is one of the most commonlyused acute stress models to explain depression and it has showngood face and predictive validity. However, despite being able toinduce depressed-like behaviors and correspondingpsychophysiological changes, there is little evidence showing thatthe LH paradigm can produce anhedonia, a core symptom seen in allforms of depression in humans. So far a couple of studies showedthat rodents bred for helplessness develop anhedonic-like behaviorsin response to stress; yet, to the best of our knowledge, nosimilar human research has tried to investigate the directrelationship between the LH model and anhedonia. In the presentstudy, we use a modified version of the original LH task toexperimentally and temporarily induce learned helplessness incollege students and then examine if the human LH paradigm inducesanhedonia. We aim to 1: address the ill-defined connection betweenthe LH model and anhedonia, and 2: directly assess helplessness inhumans as opposed to the majority of non-human animal subjects usedin the helplessness literature. We believe that our study will fillan important gap in the learned helplessness model literature, andwill advance our understanding of the relationship betweendepression and perceived control, as well as place limitations towhat can and cannot be inferred from non-human animal data in thistopic.