Long-term potentiation is one of the most extensively studied forms of neuroplasticity and is considered the strongest candidate mechanism for memory and learning. The use of event-related potentials and sensory stimulation paradigms has allowed for the translation from animal studies to non-invasive studies of LTP-like synaptic plasticity in humans. Accumulating evidence suggests that synaptic plasticity as measured by stimulus-specific response modulation is reduced in neuropsychiatric disorders such as major depressive disorder, bipolar disorders and schizophrenia, suggesting that impaired (...) class='Hi'>synaptic plasticity plays a part in the underlying pathophysiology of these disorders. This is in line with the neuroplasticity hypothesis of depression, which postulate that deficits in neuroplasticity might be a common pathway underlying depressive disorders. The current study aims to replicate and confirm earlier reports that visual stimulus-specific response modulation is a viable probe into LTP-like synaptic plasticity in a large sample of healthy adults. Further, this study explores whether impairments in LTP-like synaptic plasticity is associated with self-reported subclinical depressive symptoms and stress in a healthy population. Consistent with prior research, the current study replicated and confirmed reports demonstrating significant modulation of visual evoked potentials following visual high-frequency stimulation. Current results further indicate that reduced LTP-like synaptic plasticity is associated with higher levels of self-reported symptoms of depression and perceived stress. This indicate that LTP-like plasticity is sensitive to sub-clinical levels of psychological distress, and might represent a vulnerability marker for the development of depressive symptoms. (shrink)

We propose that sleep is linked to synaptic homeostasis. Specifically, we propose that: (1) Wakefulness is associated with synaptic potentiation in cortical circuits; (2) synaptic potentiation is tied to the homeostatic regulation of slow wave activity; (3) slow wave activity is associated with synaptic downscaling; and (4) synaptic downscaling is tied to several beneficial effects of sleep, including performance enhancement.

Interest in the role of nitric oxide (NO) in the nervous system began with the demonstration that glutamate receptor activation in cerebellar slices causes the formation of a diffusible messenger with properties similar to those of the endothelium-derived relaxing factor. It is now clear that this is due to the Ca2+/calmodulin-dependent activation of the enzyme NO synthase, which forms NO and citrulline from the amino acid L-arginine. The cerebellum has very high levels of NO synthase, and although it has low (...) levels of guanylyl cyclase, cerebellar cyclic guanosine monophosphate (cGMP) levels are an order of magnitude higher than in other brain regions. A transcellular metabolic pathway is also present in the cerebellar cortex to recycle citrulline back to arginine. The NO formed binds to and activates soluble guanylyl cyclase to elevate cGMP levels in target cells. Studies employing NADPH-diaphorase, a selective histochemical marker for NO synthase, together with immunohistochemistry, in situ hybridization and biochemical studies have indicated that NO production occurs in granule and basket cells in the cerebellar cortex, whereas cGMP formation appears to occur largely in other cells, including Purkinje cells. Given that a long-term depression of AMPA currents can be seen in isolated Purkinje cells, this anatomical localization suggests that NO cannot play an essential role in the induction of this form of synaptic plasticity. (shrink)

Preoccupation with LTP as a putative memory mechanism may have retarded the consideration of pathological modulation of synaptic plasticity in clinical disorders where memory dysfunction is not a primary feature. Encouraged by Shors & Matzel's review, we consider the relationship between stress, synaptic plasticity, and depressive disorder.

The cellular basis of motor learning in the cerebellum has been attributed mostly to long-term depression (LTD) at excitatory parallel fiber (PF)-Purkinje cell (PC) synapses. LTD is induced when PFs are activated in conjunction with a climbing fiber (CF), the other excitatory input to PCs. Recently, by using whole-cell patch-clamp recording from PCs in cerebellar slices, a new form of synaptic plasticity was discovered. Stimulation of excitatory CFs induced a long-lasting (usually longer than 30 min) of 30 sec) (...) and the durations of RP (>30 min) strongly suggests that some intracellular biochemical machinery is involved. Pharmacological evidence suggests that protein kinases are involved in RP of inhibitory synapses and LTD of excitatory PF synapses. Besides the well-described LTD, RP could be a cellular mechanism that plays an important role in motor learning. (shrink)

Long‐term potentiation and long‐term depression are thought to be cellular mechanisms contributing to learning and memory. Although the physiological phenomena have been well characterized, little consensus of their underlying molecular mechanisms has emerged. One reason for this may be the under‐appreciated complexity of the signaling pathways that can arise if key signaling molecules are discretely localized within the synapse. Recent findings suggest an unanticipated degree of structural organization at the synapse, and improved methods in cellular imaging of living tissue (...) have provided much‐needed information about the intracellular dynamics of Ca2+, thought to be critical for both LTP and LTD. In this review, we briefly summarize some of these developments, and show that a more complete understanding of cellular signaling depends on the successful integration of traditional biochemistry and molecular biology with the spatial and temporal details of synaptic ultrastructure. Biophysically realistic computer simulations can have an important role in bridging these disciplines. BioEssays 24:1130–1144, 2002. © 2002 Wiley‐Periodicals, Inc. (shrink)

Localist models of spreading activation (SA) and models assuming distributed representations offer very different takes on semantic priming, a widely investigated paradigm in word recognition and semantic memory research. In this study, we implemented SA in an attractor neural network model with distributed representations and created a unified framework for the two approaches. Our models assume a synaptic depression mechanism leading to autonomous transitions between encoded memory patterns (latching dynamics), which account for the major characteristics of automatic semantic (...) priming in humans. Using computer simulations, we demonstrated how findings that challenged attractor‐based networks in the past, such as mediated and asymmetric priming, are a natural consequence of our present model’s dynamics. Puzzling results regarding backward priming were also given a straightforward explanation. In addition, the current model addresses some of the differences between semantic and associative relatedness and explains how these differences interact with stimulus onset asynchrony in priming experiments. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Hermeneutics, Neuroscience and PsychiatryMichael T. H. Wong, MBBS, MD, MA, MDiv, PhD, FRCPsych, FRANZCP, FHKAM (bio)Hermeneutic practice in mental health has been a theme in Philosophy, Psychiatry, & Psychology (PPP) since its very beginnings. In this essay I argue that hermeneutics, the theory and practice of interpretation, promotes therapeutic interaction between mental health professionals, patients and their family.Why does this patient present in such a way at this particular (...) point in time? The distressing symptoms are there. The changes in behavior are obvious. Impairments of functions are hurting. A mental illness clearly runs in the family. There were early losses of loved ones, physical abuse at home, bullying by peers and self-medication with drugs and alcohol. Three in four adults with a mental illness first experienced that before they turned 24. The brain goes through major reorganization during adolescence and early adulthood. If synaptic pruning went wrong, psychoses emerged. When stresses activated the hypothalamic–pituitary–adrenal axis the elevated cortisol level impacted the size and function of the hippocampus and amygdala in the genetically vulnerable; anxiety, depression, bipolar, and personality disorders developed. The patient needs a voice/language to describe all these experiences and events and the psychiatrist needs a discourse to make sense of them.Eisenberg laments the swings between "brainlessness" and "mindlessness" in psychiatry. Engel argues for a "biopsychosocial" discourse. The major challenge for psychiatry is how to organize clinical information of different nature (categories, dimensions, narratives; i.e., objective vs. subjective, personal vs. interpersonal) into a coherent and comprehensible account for us all. Mental illnesses are not only neuropsychiatric spectrum disorders but also dysfunctions of social relationship and environmental/ecological adaptation. Psychiatry as a clinical neuroscience per se lacks the semantics to address the rich interactions between the physical, psychological, social, cultural, and spiritual in the illness experience of our patients. Explanation in the diagnostic formulation (objective scientific discourse on cause and effect) and understanding in the patient narrative (subjective ordinary everyday discourse on significance and meaning) are irreducible to each other (Wong, 2018). They instead interact with one another to achieve an integrative formulation, not through merging different discourses into a single assertion/monologue but via the dialectic/dialogue of "explaining more in order to understand better," as Ricoeur puts it, and between "the whole and the parts," as Schleiermacher highlights.This "therapeutic hermeneutic circle" of "explanation vs understanding" and "the whole vs the parts" includes symptoms behavior function and life events. It correlates between bio-psychosociocultural-spiritual dimensions/perspectives and does not reduce them to any particular/single [End Page 13] stance. The whole integrates the parts and the parts enrich the whole. It explains but does not explain away. It understands through an articulation of meaning and significance. This discourse is a multilayered (bio-psycho-social-cultural-spiritual) personal narrative that formulates diagnosis and care in a correlative (linking different voices/discourses) and non-reductive (no particular voice/discourse is prejudiced against) manner that is comprehensible to us all (Wong, 2021).PPP will be an excellent forum for discussing clinical hermeneutics in the future. In this digital era of social media and virtual reality, hermeneutics has the never-ending task to tackle the unprecedented challenges to meaning illness and health posed by polarizing discourses.Michael T. H. Wong Michael T.H. Wong, MBBS, MD, MA, MDiv, PhD, FRCPsych, FRANZCP, FHKAM, is Hon Clinical Professor, Department of Psychiatry, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, HKSAR, China. Michael is Chair, Section of Philosophy & Humanities in Psychiatry, World Psychiatric Association. He is an Organizational Partner & International Lead with The Collaborating Centre for Values-Based Practice in Health and Social Care, St Catherine's College Oxford. He is Advisor to the Chinese Health Foundation of Australia.ReferencesWong M. T. H. (2018). Ricoeur and the third discourse of the person: From philosophy and neuroscience to psychiatry and theology. London: Lexington Books. Google ScholarWong, M. T. H. (2021). Values, meanings, hermeneutics and mental health. In Stoyanov, D., Fulford, K. M. W. F., Stanghellini, G., Van Staden, W., & Wong, M. TH. (Eds.), International perspectives in values-based mental health practice: Case studies and commentaries (pp. 341–349... (shrink)

Deep brain stimulation (DBS) of the globus pallidus interna and subthalamic nucleus has restored some degree of motor control in many patients in advanced stages of Parkinson’s disease. DBS has also been used to treat dystonia, essential tremor (progressive neurological condition causing trembling), chronic pain, obsessive-compulsive disorder, Tourette’s syndrome, major depressive disorder, obesity, cerebral palsy, and the minimally conscious state. Although the underlying mechanisms of the technique are still not clear, DBS can modulate underactive or overactive neural circuits and restore (...) disrupted communication between and among groups of neurons in interacting regions of the brain. This can control and relieve many symptoms associated with a range of neurological and psychiatric disorders.But the procedures of implanting and stimulating the electrodes are brain-invasive and entail significant risks. Some patients receiving DBS have experienced intracerebral hemorrhage, infection, cognitive disturbances such as impulsive behavior, and affective disturbances such as mania. It is not known whether continuous electrical stimulation of the brain would reshape synaptic connectivity and permanently alter neural circuits in ways that may not be salutary. The risk of these effects indicates that DBS should be used only when a patient’s condition is refractory to all other interventions and when there is a high probability that the technique will benefit the patient and improve his or her quality of life. If a patient’s quality of life is poor and all other treatment options have been exhausted, then the likelihood of benefit can justify physicians’ exposing patients to some risk. The clinical and ethical significance of the risk in DBS underscores the obligation of physicians to obtain fully informed consent from patients undergoing the procedure. (shrink)

The vestibulo-ocular reflex (VOR) adaptation is an ideal model for investigating how the neurosteroid 17 beta-estradiol (E2) contributes to the modification of behavior by regulating synaptic activities. We hypothesized that E2 impacts VOR adaptation by affecting cerebellar synaptic plasticity at the parallel fiber–Purkinje cell (PF) synapse. To verify this hypothesis, we investigated the acute effect of blocking E2 synthesis on gain increases and decreases in adaptation of the VOR in male rats using an oral dose (2.5 mg/kg) of (...) the aromatase inhibitor letrozole. We also assessed the effect of letrozole on synaptic plasticity at the PF synapse in vitro, using cerebellar slices from male rats. We found that letrozole acutely impaired both gain increases and decreases adaptation of the VOR without altering basal ocular-motor performance. Moreover, letrozole prevented long-term potentiation at the PF synapse (PF-LTP) without affecting long-term depression (PF-LTD). Thus, in male rats neurosteroid E2 has a relevant impact on VOR adaptation and affects exclusively PF-LTP. These findings suggest that E2 might regulate changes in VOR adaptation by acting locally on cerebellar and extra-cerebellar synaptic plasticity sites. (shrink)

This pioneering book explores in depth the role of neurotransmitters in conscious awareness. The central aim is to identify common neural denominators of conscious awareness, informed by the neurochemistry of natural, drug induced and pathological states of consciousness. Chemicals such as acetylcholine and dopamine, which bridge the synaptic gap between neurones, are the 'neurotransmitters in mind' that form the substance of the volume, which is essential reading for all who believe that unravelling mechanisms of consciousness must include these vital (...) systems of the brain.Up-to-date information is provided on: Psychological domains of attention, motivation, memory, sleep and dreaming that define normal states of consciousness. Effects of chemicals that alter or abolish consciousness, including hallucinogens and anaesthetics. Disorders of the brain such as dementia, schizophrenia and depression considered from the novel perspective of the way these affect consciousness, and how this might relate to disturbances in neurotransmission.(Series B). (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Philosophy, Psychiatry, & Psychology 12.3 (2005) 235-237 [Access article in PDF] Determined by Chaos: The Nonlinear Dynamics of Free Will Jessica Wahman Keywords free will, chaos theory, determinism, materialism In "antidepressants and the Chaotic Brain: Implications for the Respectful Treatment of Selves," Douglas Heinrichs provides an intriguing justification of individuated and longer term therapy for depressive clients. He does not reject medication as a therapeutic strategy, nor does he (...) question the materialist basis of the traditional medical model. Rather, he offers a physically deterministic account of depression that is at the same time compatible with a sense of human agency and individuality. Heinrichs suggests that human physiology and its psychiatric disorders are better accounted for by the nonlinear dynamics of chaos theory than by the traditional account of neurotransmitter production and reuptake. Because the latter, microscopic, explanation suggests a direct cause-and-effect relationship between synaptic activity and subjective affect, it cannot account for the wide variation of responses to the same medications, nor can it satisfy the client's fears that her drug-induced well-being is not fully hers to control. Chaos theory, he asserts, can provide a better explanation by treating the human organism as a complex holistic system whose patterns resemble a topographical map of probability more than they do a unidirectional vector model of cause to effect. Like the weather, human affect and behavior are physically determined but difficult to predict, and so careful attention to both the individual history of the client and the uniqueness of responses to medication are a necessary part of any successful therapeutic program.Connected to this theory of nonlinear physiology is Heinrichs's account of autonomy and agency under this rubric. He notes that a psychology based on chaos theory is not only compatible with the notion of free will, it can better explain why the successful use of medication actually increases freedom and autonomy instead of limiting it. It is here that I wish to focus my comments, because his interpretation of free will may give us, to borrow a phrase from Daniel Dennett, a "variet[y] of free will worth wanting" (1984, title page). Free will, in this case, is not a metaphysical ability to act above and beyond our material causes, but is instead a property of the material system itself, namely when that system feels itself capable of greater psychic mobility around the topographical map of probabilistic patterns.According to this model, our ability to reason, plan, and act on the decisions we make is itself a [End Page 235] part of our chaotically determined neurologic system. When we are healthy, we are able to reason in our best interests and act on those reasons. This is modeled as an ability for the organism to metaphorically "move about" the map of its own possibilities, and more important, to both enter and escape certain states, known as chaotic attractors, into which it is likely to be drawn. "Where" we wind up, psychologically speaking, at any point in time is determined by our own system, and so we may say that in such a case we are autonomous and our choices are made freely. Depression, on the other hand, can be compared to a deep groove in the map, a chaotic attractor that is hard to escape, and so the system quite literally becomes "stuck in a rut." This is subjectively experienced as the tendency for thought processes and activities to fall into negative and self-defeating patterns despite the best efforts of the client to escape these habits. So long as the organism does not have a sense of being "trapped" in an attractor (whether a depressive or, for example, manic or compulsive state), then that organism may be said to be free. Medication and the therapy that accompanies it, so far as it facilitates our ability to escape deep chaotic attractors, promotes our own freedom of will. If a car cannot spin its way out of a ditch, does the tow truck hinder or promote its freedom by hauling it back onto solid pavement where it may again... (shrink)

How do human infants learn the causal dependencies between events? Evidence suggests that this remarkable feat can be achieved by observation of only a handful of examples. Many computational models have been produced to explain how infants perform causal inference without explicit teaching about statistics or the scientific method. Here, we propose a spiking neuronal network implementation that can be entrained to form a dynamical model of the temporal and causal relationships between events that it observes. The network uses spike-time (...) dependent plasticity, long-term depression, and heterosynaptic competition rules to implement Rescorla–Wagner-like learning. Transmission delays between neurons allow the network to learn a forward model of the temporal relationships between events. Within this framework, biologically realistic synaptic plasticity rules account for well-known behavioral data regarding cognitive causal assumptions such as backwards blocking and screening-off. These models can then be run as emulators for state inference. Furthermore, this mechanism is capable of copying synaptic connectivity patterns between neuronal networks by observing the spontaneous spike activity from the neuronal circuit that is to be copied, and it thereby provides a powerful method for transmission of circuit functionality between brain regions. (shrink)

Pains that persist long after damaged tissue hasrecovered remain a perplexing phenomenon. Theseso-called chronic pains serve no useful function foran organism and, given its disabling effects, mighteven be considered maladaptive. However, a remarkablesimilarity exists between the neural bases thatunderlie the hallmark symptoms of chronic pain andthose that subserve learning and memory. Bothphenomena, wind-up in the pain literature andlong-term potentiation (LTP) in the learning andmemory literature, are forms of neuroplasticity inwhich increased neural activity leads to a longlasting increase in the excitability (...) of neuronsthrough structural modifications at pre- andpost-synaptic sites. Moreover, the synapticmodifications of wind-up and LTP share a commonmechanism: a glutamate N -methyl-D-aspartate(NMDA) receptor interaction that initiates a calciummediated biochemical cascade that ultimately enhancessignal processing at the -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor. This paper arguesthat chronic pain, which has no adaptive value, canbe accounted for in terms of the highly adaptivephenomenon of activity-dependent neural plasticity;hence, some cases of chronic pain can beconceptualized as a memory trace in spinal neurons. (shrink)

From a phenomenological viewpoint, shame and guilt may be regarded as emotions which have incorporated the gaze and the voice of the other, respectively. The spontaneous and unreflected performance of the primordial bodily self has suffered a rupture: In shame or guilt we are rejected, separated from the others, and thrown back on ourselves. This reflective turn of spontaneous experience is connected with an alienation of primordial bodiliness that may be described as a "corporealization": The lived-body is changed into the (...) objective, corporeal body or "body-for-others." The polarity of "bodiliness" and "corporeality" may further a phenomenological understanding of several mental disorders connected with shame and guilt. This is shown by the examples of body dysmorphic disorder and melancholic depression. (shrink)

BackgroundThe pandemic of Coronavirus Disease 2019 has burdened an unprecedented psychological stress on the front-line medical staff, who are at high risk of depression. While existing studies and theories suggest that factors such as gratitude, social support, and hope play a role in the risk of depression, few studies have combined these factors to explore the relationship between them.ObjectiveThis study examined the mediating roles of social support and hope in the relationship between gratitude and depression among front-line (...) medical staff during the pandemic of COVID-19.MethodsThis study used the Gratitude Questionnaire, the Perceived Social Support Scale, the State Hope Scale, and the Center for Epidemiologic Studies Depression Scale to examine the gratitude, social support, hope, and depression among 344 front-line medical workers in Wuhan, which was the hardest-hit area of COVID-19 in China.ResultsThe results showed that the prevalence of mild depressive disorder was 40.12% and the prevalence of major depressive disorder was 9.59% among front-line medical staff during the pandemic of COVID-19; gratitude has a direct and negative effect on depression. Gratitude was negative predictors of depression through the mediating variables of social support and hope [βgratitude–social support–depression = −0.096, 95%CI; βgratitude–hope–depression = −0.034, 95%CI], as well as via an indirect path from social support to hope [βgratitude–social support–hope–depression = −0.089, 95%CI ].ConclusionThe study findings indicate that gratitude as a positive emotion can reduce depression in medical staff by promoting social support and hope, respectively. Gratitude also reduced depression in health care workers through a chain mediating effect of social support and hope. Overall, gratitude can directly foster social support and hope, and protect people from stress and depression, which has implications for clinical interventions among front-line medical staff during the pandemic of COVID-19. (shrink)

Cognitive reappraisal is one of the core treatment components of cognitive behavioral therapy and is the gold standard treatment for major depressive disorders. Accumulating evidence indicates that cognitive reappraisal could function as a protective factor of cognitive vulnerability to depression. However, the neural mechanism by which CR training reduces cognitive vulnerability to depression is unclear. There is ample evidence that the prefrontal–amygdala circuit is involved in CR. This study proposes a novel cognitive bias model of CR training which (...) hypothesizes that CR training may improve the generation ability of CR with altered prefrontal–amygdala functional activation/connectivity, thus reducing negative cognitive bias and alleviating depressive symptoms. This study aims to explore whether there is abnormal CR strategy generation ability in individuals who are cognitively vulnerable to depression; test the hypothesis that CR training alleviates depressive symptoms through the mediators of cognitive bias ; explore the neural mechanism by which CR training may enhance the ability of CR strategy generation; and examine the short- and long-term effects of CR training on the reduction in depressive symptoms in individuals who are cognitively vulnerable to depression following intervention and 6 months later. The study is promising, providing theoretical and practical evidence for the early intervention of depression-vulnerable individuals. (shrink)

We estimate that 208,000 deep brain stimulation (DBS) devices have been implanted to address neurological and neuropsychiatric disorders worldwide. DBS Think Tank presenters pooled data and determined that DBS expanded in its scope and has been applied to multiple brain disorders in an effort to modulate neural circuitry. The DBS Think Tank was founded in 2012 providing a space where clinicians, engineers, researchers from industry and academia discuss current and emerging DBS technologies and logistical and ethical issues facing the field. (...) The emphasis is on cutting edge research and collaboration aimed to advance the DBS field. The Eighth Annual DBS Think Tank was held virtually on September 1 and 2, 2020 (Zoom Video Communications) due to restrictions related to the COVID-19 pandemic. The meeting focused on advances in: (1) optogenetics as a tool for comprehending neurobiology of diseases and on optogenetically-inspired DBS, (2) cutting edge of emerging DBS technologies, (3) ethical issues affecting DBS research and access to care, (4) neuromodulatory approaches for depression, (5) advancing novel hardware, software and imaging methodologies, (6) use of neurophysiological signals in adaptive neurostimulation, and (7) use of more advanced technologies to improve DBS clinical outcomes. There were 178 attendees who participated in a DBS Think Tank survey, which revealed the expansion of DBS into several indications such as obesity, post-traumatic stress disorder, addiction and Alzheimer’s disease. This proceedings summarizes the advances discussed at the Eighth Annual DBS Think Tank. (shrink)

Recently, interest in the unique pathways linking discrete positive emotions to specific health outcomes has gained increasing attention, but the role of awe is yet to be elucidated. Awe is a complex and transformative emotion that can restructure individuals' mental frames so deeply that it could be considered a therapeutic asset for major mental health major issues, including depression. Despite sparse evidence showing a potential connection between depression and awe, this link has not been combined into a proposal (...) resulting in specific intervention guidelines. The aim of this perspective was three-fold: to provide a new unifying model of awe's functioning—the Matryoshka model; to show systematic and explicit connections between this emotion and depression; and to suggest specific guidelines of intervention utilizing the potential therapeutic role of awe for mental health, specifically for depression. This theoretical endeavor in its entirety has been framed within the health domain. (shrink)

ABSTRACTThe aim of this study was to examine the extent to which cognitive emotion regulation strategies were “common or transdiagnostic correlates” of symptoms of depression and anxiety and/or “specific correlates” distinguishing one problem category from the other. The sample comprised 582 13- to 16-year-old secondary school students. Symptoms of depression and anxiety were measured by the SCL-90, and cognitive emotion regulation strategies were measured by the CERQ, in a cross-sectional design. Multivariate regression analyses were performed. Before controlling for (...) comorbidity, the same cognitive emotion regulation strategies that were related to symptoms of depression were also related to symptoms of anxiety. However, after controlling for comorbid anxiety symptoms, rumination, self-blame, positive reappraisal, and positive refocusing were uniquely associated with depression symptoms; and after controlling for comorbid depression symptoms, ca... (shrink)

The aim of the present study was to examine whether offspring at high and low familial risk for depression differ in the immediate and more lasting behavioural and physiological effects of hedonica...

Emotion differentiation has generally been viewed as a trait that is related to emotion regulation and well-being. There are theoretical considerations that state that the beneficial effect on well...

ABSTRACTThe aim of this study was to examine the extent to which cognitive emotion regulation strategies were “common or transdiagnostic correlates” of symptoms of depression and anxiety and/or “specific correlates” distinguishing one problem category from the other. The sample comprised 582 13- to 16-year-old secondary school students. Symptoms of depression and anxiety were measured by the SCL-90, and cognitive emotion regulation strategies were measured by the CERQ, in a cross-sectional design. Multivariate regression analyses were performed. Before controlling for (...) comorbidity, the same cognitive emotion regulation strategies that were related to symptoms of depression were also related to symptoms of anxiety. However, after controlling for comorbid anxiety symptoms, rumination, self-blame, positive reappraisal, and positive refocusing were uniquely associated with depression symptoms; and after controlling for comorbid depression symptoms, ca... (shrink)

The comorbidity of personality disorders and mental disorders is commonly understood through three types of theoretical models: either a) personality disorders precede mental disorders, b) mental disorders precede personality disorders, c) mental disorders and personality disorders share common etiological grounds. Although these hypotheses differ with respect to their idea of causal direction, they all imply a latent variable perspective, in which it is assumed that either personality and mental disorders are latent variables that have certain causal relations [models a) and (...) b)]; or that, as in model c), the common etiology is in fact a latent variable that causes symptomatology of both personality and mental disorders. We aim to provide another perspective on the comorbidity between personality and mental disorders, namely a network perspective. To this end, we investigated Major Depression and Borderline Personality Disorder and hypothesized that symptoms of BPD and MD could interact with one another rather than being caused by a latent variable. To illustrate this theoretical network conceptualization of the comorbidity of BPD and MD we analyzed a cross-sectional clinical dataset of 376 patients who were asked to complete the Structured Clinical Interview for DSM-IV Axis II Disorders and the Beck Depression Inventory II. The results identify direct associations between symptoms of MD and BPD. If we take the links in this empirical network to be ‘substantive', this suggests a radical shift of our current conceptualization of the comorbidity of mental disorders and personality disorders. (shrink)

In this article, I argue that depression and suicide are natural kinds insofar as they are classes of abnormal behavior underwritten by sets of stable biological mechanisms. In particular, depression and suicide are neurobiological kinds characterized by disturbances in serotonin functioning that affect various brain areas (i.e., the amygdala, anterior cingulate, prefrontal cortex, and hippocampus). The significance of this argument is that the natural (biological) basis of depression and suicide allows for reliable projectable inferences (i.e., predictions) to (...) be made about individual members of a kind. In the context of assisted suicide, inferences about the decision-making capacity of depressed individuals seeking physician-assisted suicide are of special interest. I examine evidence that depression can hamper the decision-making capacity of individuals seeking assisted suicide and discuss some implications. (shrink)

Argues that emotivism is compatible with cases where we seem to lack motivation to act according to our moral opinions.