Matching Items (6)
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- All Subjects: Resilience
- All Subjects: RASopathies
- Creators: Waldron, Vincent
Description
Chronic stress results in functional and structural changes to the hippocampus. Decades of research has led to insights into the mechanisms underlying the chronic stress-induced deficits in hippocampal-mediated cognition and reduction of dendritic complexity of hippocampal neurons. Recently, a considerable focus of chronic stress research has investigated the mechanisms behind the improvements in hippocampal mediated cognition when chronic stress ends and a post-stress rest period is given. Consequently, the goal of this dissertation is to uncover the mechanisms that allow for spatial ability to improve in the aftermath of chronic stress. In chapter 2, the protein brain derived neurotrophic factor (BDNF) was investigated as a mechanism that allows for spatial ability to show improvements following the end of chronic stress. It was found that decreasing the expression of BDNF in the hippocampus prevented spatial memory improvements following a post-stress rest period. Chapter 3 was performed to determine whether hippocampal CA3 apical dendritic complexity requires BDNF to show improvements following a post-stress rest period, and whether a receptor for BDNF, TrkB, mediates the improvements of spatial ability and dendritic complexity in a temporal manner, i.e. during the rest period only. These experiments showed that decreased hippocampal BDNF expression prevented improvements in dendritic complexity, and administration of a TrkB antagonist during the rest period also prevented the improvements in spatial ability and dendritic complexity. In chapter 4, the role of the GABAergic system on spatial ability following chronic stress and a post-stress rest period was investigated. Following chronic stress, it was found that male rats showed impairments on the acquisition phase of the RAWM and this correlated with limbic glutamic acid decarboxylase, a marker for GABA. In chapter 5, a transgenic mouse that expresses a permanent marker on all GABAergic interneurons was used to assess the effects of chronic stress and a post-stress rest period on hippocampal GABAergic neurons. While no changes were found on the total number of GABAergic interneurons, specific subtypes of GABAergic interneurons were affected by stressor manipulations. Collectively, these studies reveal some mechanisms behind the plasticity seen in the hippocampus in response to a post-stress rest period.
ContributorsOrtiz, J. Bryce (Author) / Conrad, Cheryl D. (Thesis advisor) / Newbern, Jason M. (Committee member) / Orchinik, Miles (Committee member) / Sanabria, Federico (Committee member) / Arizona State University (Publisher)
Created2018
Description
Abstract Communication scholars have begun to contribute to the theoretical understanding of resilience as a dynamic and collaborative process, which can be talked into being (Buzzanell, 2010). Previous research has examined the role of resilience in romantic couples, however, has focused disproportionately on heterosexual couples. This offers a limited, and singular understanding of how resilience is developed and sustained in romantic relationships. To better understand the scope and breadth of resilience, this study examined five same-sex couples through an in-depth qualitative case study analysis. The purpose of this study was to contribute to the small body of existing data, as well as, enhance our understanding of how resilience works in other contexts. Data was analyzed for thematic patterns, and compared to existing data on same-sex relationships. The findings supported that resilience is a collaborative process that is facilitated by communication. There were some discrepancies from the data collected in this study compared to previous findings; however, due to the small sample size, findings from this study cannot be generalized to the larger population.
ContributorsHartt, Cori Ann (Author) / Waldron, Vincent (Thesis director) / Kelley, Doug (Committee member) / Barrett, The Honors College (Contributor) / School of Social and Behavioral Sciences (Contributor)
Created2015-05
Description
Rasopathies are a family of developmental syndromes that exhibit craniofacial abnormalities, cognitive disabilities, developmental delay and increased risk of cancer. However, little is known about the pathogenesis of developmental defects in the nervous system. Frequently, gain-of-function mutations in the Ras/Raf/MEK/ERK cascade (aka ERK/MAPK) are associated with the observed pathogenesis. My research focuses on defining the relationship between increased ERK/MAPK signaling and its effects on the nervous system, specifically in the context of motor learning. Motor function depends on several neuroanatomically distinct regions, especially the spinal cord, cerebellum, striatum, and cerebral cortex. We tested whether hyperactivation of ERK/MAPK specifically in the cortex was sufficient to drive changes in motor function. We used a series of genetically modified mouse models and cre-lox technology to hyperactivate ERK/MAPK in the cerebral cortex. Nex:Cre/NeuroD6:Cre was employed to express a constitutively active MEK mutation throughout all layers of the cerebral cortex from an early stage of development. RBP4:Cre, caMEK only exhibited hyper activation in cortical glutamatergic neurons responsible for cortical output (neurons in layer V of the cerebral cortex). First, the two mouse strains were tested in an open field paradigm to assess global locomotor abilities and overall fitness for fine motor tasks. Next, a skilled motor reaching task was used to evaluate motor learning capabilities. The results show that Nex:Cre/NeuroD6:Cre, caMEK mutants do not learn the motor reaching task, although they performed normally on the open field task. Preliminary results suggest RBP4:Cre, caMEK mutants exhibit normal locomotor capabilities and a partial lack of learning. The difference in motor learning capabilities might be explained by the extent of altered connectivity in different regions of the corticospinal tract. Once we have identified the neuropathological effects of various layers in the cortex we will be able to determine whether therapeutic interventions are sufficient to reverse these learning defects.
ContributorsRoose, Cassandra Ann (Author) / Newbern, Jason M. (Thesis director) / Olive, Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
Description
The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for the differentiation of Embryonic Stem Cells (ESC) into neuronal precursors (Li z et al, 2006). ERK signaling has also shown to mediate Schwann cell myelination of the peripheral nervous system (PNS) as well as oligodendrocyte proliferation (Newbern et al, 2011). The class of developmental disorders that result in the dysregulation of RAS signaling are known as RASopathies. The molecular and cell-specific consequences of these various pathway mutations remain to be elucidated. While there is evidence for altered DNA transcription in RASopathies, there is little work examining the effects of the RASopathy-linked mutations on protein translation and post-translational modifications in vivo. RASopathies have phenotypic and molecular similarities to other disorders such as Fragile X Syndrome (FXS) and Tuberous Sclerosis (TSC) that show evidence of aberrant protein synthesis and affect related pathways. There are also well-defined downstream RAS pathway elements involved in translation. Additionally, aberrant corticospinal axon outgrowth has been observed in disease models of RASopathies (Xing et al, 2016). For these reasons, this present study examines a subset of proteins involved in translation and translational regulation in the context of RASopathy disease states. Results indicate that in both of the tested RASopathy model systems, there is altered mTOR expression. Additionally the loss of function model showed a decrease in rps6 activation. This data supports a role for the selective dysregulation of translational control elements in RASopathy models. This data also indicates that the primary candidate mechanism for control of altered translation in these modes is through the altered expression of mTOR.
ContributorsHilbert, Alexander Robert (Author) / Newbern, Jason (Thesis director) / Olive, M. Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
Description
The objective of this project was to develop a forgiveness training program to be used at a corporate level in addition to the current conflict management strategies. In addition to teaching the value of forgiveness, this search also touches on resilience and how forgiveness increases our personal resiliency. Forgiveness and resilience have been closely linked in previous forgiveness research as they relate to reconciliation. Based on the research, forgiveness has been widely talked about in relation to religious practices, however it is now being discussed in relation to communication. In order to understand forgiveness as a communication process, one has to understand where it began and how the definition of forgiveness has evolved overtime. This project looks at how forgiveness creates value for the individual in terms of the relationship and expresses why forgiveness and reconciliation are not mutually exclusive. Forgiving an individual does not always lead to reconciling the relationship; however, making it so the individuals can continue working together is the goal at work. A key part of understanding forgiveness is being able to identify what forgiveness is not, as much of what we have been taught from a young age is the exact opposite. Adult learners are much different from any other type of learners due to the level of life experience they have -- which can often make it more challenging to rewrite concepts, like forgiveness. This project identifies the best ways to teach adult learners through the use of interactive handouts and videos that demonstrate the power of forgiveness in our day-to-day lives.
ContributorsKartes, Chloe Verginia (Author) / Waldron, Vincent (Thesis director) / Kelley, Douglas (Committee member) / School of Social and Behavioral Sciences (Contributor, Contributor) / W. P. Carey School of Business (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
Description
Suicidality, understood as the risk of suicide with intent or the idea of suicide, has been increasingly prevalent in our country, yet the topic of suicidality is one that is often spoken in hushed tones and behind closed doors (Pam, 2013). While suicide statistics trend upwards, there is a growing need to understand representations of suicidality, particularly within media (Centers for Disease Control, 2017). This thesis looks to explore the representations of suicidality in media, specifically Netflix’s original series, Thirteen Reasons Why. Data collection for this thesis will be collected from online social media forums dedicated to the show in the form of episode discussions reflecting on each episode in the season. Through an emergent, grounded analysis, this paper will address current representations of suicidality within Thirteen Reasons Why as well as identify common themes found in online social media forums. This research established common themes of resilience-enhancing, community building, and individuals feeling at-risk or triggered by representations of suicidality in Thirteen Reasons Why as found throughout the online social media forums.
ContributorsTaylor, Katlyn (Author) / Nadesan, Majia H (Thesis advisor) / Walker, Michael (Committee member) / Waldron, Vincent (Committee member) / Arizona State University (Publisher)
Created2020