Der Weg von der Diagnose einer Depression, bis hin zu einer adäquaten Therapie, ist oft eine langer. Der Hausarzt ist dabei zumeist der erste Ansprechpartner. Sulz & Deckert (2012) haben zur Durchführung einer psychiatrischen Kurz-Psychotherapie Psychotherapiekarten zur Anwendung durch Ärzte in ihrer Sprechstunde entwickelt. Ihre Wirksamkeit wurde in der ambulanten Psychotherapie bereits bestätigt, jedoch die Möglichkeit ihrer Anwendung im hausärztlichen Bereich bislang noch nicht untersucht. Diese Dissertation soll prüfen, ob sich die Sprechstundenkarten, im hausärztlichen Setting, effektiv einsetzen lassen und ob generell der Bedarf an einer solchen Methodik seitens der Hausärzte besteht. / The journey from diagnosis of depression to adequate treatment is often a long one. The general practitioner is usually the first point of contact. Sulz & Deckert (2012) developed psychotherapy cards for use by physicians in their consultation hours to perform a psychiatric short-term psychotherapy. Its effectiveness has already been confirmed in outpatient psychotherapy, but the possibility of its use in general medicine has not yet been investigated. The aim of this dissertation is to examine whether the consultation cards can be used effectively in the general practitioner setting and whether there is a general need for such a methodology on the part of general practitioners.

Research has supported the efficaciousness of mindfulness-based interventions on depression and general psychological well-being (Teasdale et al., 2000). Thus, researchers are beginning to examine the specific mechanisms of mindfulness's salutary effects (Shapiro, Carlson, Astin, & Freedman, 2006). As mindfulness has been increasingly linked to enhanced emotional awareness and emotion regulation (Nielsen & Kaszniak, 2006; Chambers Gullone, & Allen, 2009), the specific act of objectively labeling affective experience has been proposed as an emotion regulation mechanism of mindfulness. Research has linked emotion regulation pathways in the brain with experimental tasks of affect labeling in individuals with high trait mindfulness (Creswell, Way, Eisenberger, & Lieberman, 2007). The aim of this study was to examine affect labeling as an emotion regulation mechanism of mindfulness in the context of well-established cognitive models of depression. Specifically, the study investigated whether individuals asked to label facial stimuli with affective labels recovered from a negative mood more quickly, and with more emotional granularity, than those in a control condition. One hundred and forty-nine Temple University undergraduates completed measures of mood, emotion regulation, and cognitive style prior to a negative mood priming task and were randomly assigned to one of two labeling conditions: affect labeling or gender labeling (control). Emotion dysregulation proved to be an important predictor of affective response to the mood induction. Specifically, emotion dysregulation was positively associated with negative affect, and negatively associated with positive affect, preceding and following the mood induction. However, contrary to study hypotheses, HLM analyses indicated that speed and specificity of affective recovery did not differ across experimental condition; thus, affect labeling was not associated with more adaptive emotional regulation. In addition, cognitive styles and mindfulness failed to moderate the relationship between affect labeling and affective recovery in the expected direction. However, greater trait mindfulness was associated with less negative affective responses to the mood induction. Implications of study findings, strengths and limitations of the study, as well as future directions are discussed. / Psychology

Affecting one in every eight Canadian men, prostate cancer is the most common type of cancer among males. As with other forms of cancer, men with prostate cancer are much more likely to develop comorbid depression than the general population without cancer diagnoses. Depression negatively affects these men’s quality of life and increases mortality rates among cancer patients. Therefore, effective therapies to manage depression in this unique subpopulation are needed. This project sets out to assess the efficacy of glutamate-targeting drugs as antidepressants. The major excitatory neurotransmitter in the central nervous system, glutamate is released in excessive quantities by cancer cells. It is thought that this abundance of glutamate leads to excitotoxicity and neurodegeneration, affecting neurons in important regions of the brain relating to mood and mood regulation. A validated mouse model of depression was established using RM1 murine prostate cancer cells. This model was then used to test the properties of three drugs: sulfasalazine (SSZ), (S)-4-carboxyphenylglycine ((S)-4-CPG), and 2,3-dioxo-6-nitro-1,2,3,4-tetrahydro-benzo[f]quinoxaline-7-sulfonamide (NBQX). Results show that these drugs were able to improve depressive-like behaviours and symptoms to varying degrees, at least partially reversing the negative effects of tumours. This project showed that disrupting glutamate release and/or signaling could be an effective approach for an antidepressant therapy or adjuvant in prostate cancer patients. / Thesis / Master of Science (MSc) / Prostate cancer affects one in every eight Canadian men. Cancer patients are at a much higher risk of developing depression than the rest of the population. Unfortunately, current antidepressants are limited in their ability to improve depressive symptoms in cancer patients. Therefore, this project sets out to identify new options for treating depression in prostate cancer patients. Glutamate is a signalling molecule that is released in abundance by cancer cells and is largely responsible for communication between neurons in the central nervous system. This project showed that limiting the amount of glutamate released by cancer cells and limiting glutamate-based signaling improves depressive-like symptoms in mice with prostate cancer tumours. These results suggest that targeting glutamate could be an effective antidepressant therapy in the cancer population.

Information is believed to be stored in the brain by constructing new neural circuits, and these circuits are shaped by changes in the strength of the synaptic connections between the neurons making up the circuit. According to most theories of memory, new circuits can be formed by either increasing or decreasing the strength of synaptic connections. Bidirectional modifications in synaptic efficacy are also central components in recent computer simulations of learning and memory. While long-term potentiation (LTP) has been the focus of extensive research into the mechanisms underlying information storage in the mammalian brain, long-term depression (LTD) and depotentiation, its depressive counterparts, have not. Furthermore, most of the LTD research has involved the use of anaesthetized animals and in vitro slice preparations, making it more difficult to determine the role of this synaptic phenomenon in learning and memory in the intact behaving animal. This thesis provides the first detailed examination of: 1) the induction and decay of both LTD and depotentiation in the neocortex of the awake, freely moving animal; 2) the effects of N-methyl D-Aspartate receptor (NMDAR) blockade on the induction of LTD, LTP, and depotentiation (NMDA receptor activation is known to play a major role in most forms of LTP); and 3) the interactions between these synaptic phenomena. LTD was expressed as a significant reduction in the amplitude of both short and long-latency field potential components. Depotentiation was expressed as a long lasting decrease in the amplitude of a previously enhanced late component. LTD was found to be greater in magnitude and longer lasting when the conditioning stimulation was repeated. However, unlike LTP induction, the conditioning stimulation was equally effective whether spaced over hours or days. NMDA receptor antagonism blocked LTP induction and instead produced a depression effect similar to LTD. Unlike LTP, LTD and depotentiation were found to be NMDAR-independent in the neocortex of the freely moving rat. LTP and LTD are both reversible phenomena and LTD-inducing stimulation can modulate the effects of LTP-inducing stimulation. LTD-inducing stimulation, when delivered following to LTP-inducing stimulation, attenuates the induction rate for potentiation. LTD and depotentiation may play important roles in the ongoing experience-induced modification of neuronal connectivity. Furthermore, these results are consistent with the hypothesis that potentiation and depression reflect the physiological instantiation of a bidirectional learning rule. / Thesis / Doctor of Philosophy (PhD)

No description available.

Men as well as women are affected by the life-changing events of pregnancy and childbirth. The nature of fatherhood and the role of the male in the birthing process have undergone significant changes in the past several decades. While this phenomenon has been well-documented regarding the changes a father experiences during a healthy pregnancy and birth, there is little research that addresses the implications for the man when his spouse or partner is diagnosed with postpartum depression. Approximately 10 to 20% of birth mothers are affected by some form of this disorder (Greenberg & Springen, 2001). The literature on this topic has grown steadily in an effort to better understand the reasons and implications of such a diagnosis for a woman. This researcher's intent was to identify the perspectives of men whose spouses or partners were diagnosed with postpartum depression. Understanding this situation from their perspectives can represent information regarding the effects of postpartum depression on the interpersonal relationship and, secondarily, the family unit. In particular, relationship strains between the men and their spouses or partners and the impact on the adjustment to having an infant to care for were explored. Medical records were reviewed in a medical practice for significant scores on the mother's Edinburgh Postnatal Screening Scale. After a series of elimination steps, seven men were identified and willing to participate in the research. In an hour-long interview, the men discussed their experience with their spouse/partner's postpartum depression. Field notes were taken before, during and immediately following the interviews to add clarification, using nonverbal responses to the setting and interview questions. The transcripts of the interviews were coded to identify common categories, which in turn generated themes of emotional deregulation, seeking normalcy, understanding self, and disappointment. Anger was noted by the seven men as a response on several levels to the postpartum depression. In addition to anger, frustration was expereinced with the lack of information received and the lack of response from the medical community as a whole. Several of the men reported surprise at their previous emotions resurfacing so readily when answering the interview questions. / Ph. D.

Major Depressive Disorder is a common mood disorder, affecting more than 300 million people worldwide. Stress, being a potent trigger for various mood disorders, including depression, affects both the peripheral and central immune systems. Microglia are the resident immune cells in the brain and changes in their morphology and state of activation in response to stress have been reported in a number of brain regions, however most studies examined only male subjects. In our studies we investigated morphological changes in microglia in the nucleus accumbens and subregions of the hippocampus in both male and female mice following variable stress. Our findings demonstrate that following 6 days of variable stress female microglia acquire a more activated phenotype compared to microglia in males. These sex specific effects in microglia activation were also observed in the nucleus accumbes, but not the dentate gyrus after 28 days of stress. Utilizing a number of pharmacological agents, we further investigated whether changes in the inflammatory states of microglia modulate behavior in female mice in a variable stress model for depression. We found that rosiglitazone, peroxisome proliferator activated receptor gamma PPAR) agonist, which causes microglial shift to an anti-inflammatory state, conferred social resilience in female mice after 6 days of variable stress. We further demonstrated that blocking pro-inflammatory activation of microglia with minocycline, a tetracyclic antibiotic, did not prevent the stress effects on behavior. Surprisingly, prior pro-inflammatory activation of microglia with lipopolysaccharide (LPS), an endotoxin from gram-negative bacteria, was protective against subsequent variable stress. Finally, I describe the impact of systemic application of these drugs on microglia morphology and activation state, and cytokine levels in the nucleus accumbens of female mice. Taken together this body of work contributes to a growing number of studies demonstrating neuro-immune mechanisms associated with depression. / Doctor of Philosophy / Major Depressive Disorder is a debilitating mood disorder, affecting more than 300 million people worldwide. The prevalence of MDD is higher in women than men, and women make up a higher percentage of patients with treatment resistant depression. Furthermore, men and women, diagnosed with depression, experience different symptoms, suggesting there might be sex specific mechanisms in susceptibility and development of depression. Stress, being a potent trigger for various mood disorders, including depression, affects both the peripheral and central immune systems, including microglia, the resident immune cells of the brain. In this work, I investigated the impact of stress on microglia activation in the nucleus accumbens and hippocampus, brain regions associated with depression, and found sex differences in activation of microglia following variable stress. To further understand the role of microglial in development of depression we conducted a number of different experiments, pharmacologically manipulating the activation state of microglia in the nucleus accumbens in female mice. We found that shifting microglia to an anti-inflammatory state promoted social resilience in female mice after 6 days of variable stress. We further demonstrated that blocking pro-inflammatory activation of microglia did not prevent the stress effects on behavior. Surprisingly, prior pro-inflammatory activation of microglia was protective against subsequent variable stress. Taken together this work contributes to a growing number of studies demonstrating neuro-immune mechanisms associated with depression.

The purpose of the current study was to examine a model explaining a pathway from anxiety to depression in youth. Additionally, a second model was considered examining specifically the worry component of anxiety and its role in the development of depression. Path analyses were used to examine the relationships between general anxiety and worry and academic competence and functioning, social competence and functioning, attributional style, hopelessness, and depression. In addition, the impact of sex and cognitive ability on these relationships was examined. Results revealed that anxious and depressive symptomatology were significantly correlated. Further, some support was found to suggest that the significant relationship between self-reported anxiety and depression was partially mediated through social and/or academic variables as well as attributional style and hopelessness. While sex was not found to significantly impact these relationships, cognitive ability did moderate the relationship between worry and academic functioning even when other variables were considered simultaneously. The implications of these findings for treatment and research are discussed. / Ph. D.

No / The concepts of “defeat” (representing failed social struggle) and “entrapment” (representing an inability to escape from a situation) have emerged from the animal literature, providing insight into the health consequences of low social rank. Evolutionary models suggest that these constructs co-occur and can lead to the development of mental disorders, although there is limited empirical evidence supporting these predictions. Participants (N=172) were recruited from economically deprived areas in North England. Over half of participants (58%) met clinical cut-offs for depression and anxiety, therefore we conducted analyses to establish whether participant outcomes were dependent on baseline defeat and entrapment levels. Participants completed measures of defeat, entrapment, depression and anxiety at two time-points twelve months apart. Factor analysis demonstrated that defeat and entrapment were best defined as one factor, suggesting that the experiences co-occurred. Regression analyses demonstrated that changes in depression and anxiety between T1 and T2 were predicted from baseline levels of defeat and entrapment; however, changes in defeat and entrapment were also predicted from baseline depression and anxiety. There are implications for targeting perceptions of defeat and entrapment within psychological interventions for people experiencing anxiety and depression and screening individuals to identify those at risk of developing psychopathology.

Yes / During the excavation season in 2018, I experienced a depressive episode on site and struggled to maintain productivity with the rest of my team. I felt like I wasn't a "real" archaeologist, and turned to Twitter to vent about my situation using the hashtag #DiggingWhileDepressed. To my surprise, others used the hashtag to express their own feelings about mental wellness (or lack thereof) in archaeology. Now that discussion has started, this paper will propose the next steps for our discipline to tackle this pertinent issue. By challenging the toxic masculinity and ableism inherent in the way we view archaeological labour, I will posit tangible ways in which we, as archaeologists, can support each other on and off the field.