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- Creators: Olive, Foster
- Creators: School of Criminology and Criminal Justice
- Member of: Barrett, The Honors College Thesis/Creative Project Collection
Description
Introduction: Depression is one of the most prevalent mental illnesses in the United States, and is characterized by feeling sad or empty most of the day, nearly every day (American Psychiatric Association, 2013). The experience of childhood trauma is one of many factors that may lead to depression, while trauma can also yield other adverse life outcomes, such as alcohol-related consequences (Felitti et al., 2001; Neumann, 2017). One of the specific aims of this investigation was to examine the direct influences of childhood trauma on depression. We also examined selected direct and indirect influences of childhood trauma on drinking outcomes through the potential mediating mechanism of depression. We examined three distinct drinking outcomes, 1) impaired control over drinking (i.e. the inability to stop drinking when intended), 2) heavy episodic drinking (four or more drinks on one occasion for men, four or more for women), and 3) alcohol-related problems. Methods: A survey was administered to 940 (466 women, 474 men) university students. Structural equation modeling was used to examine the data. Potential two- and three-path mediated effects were examined with the bias corrected bootstrap technique in Mplus (MacKinnon, 2008). Results: Emotional abuse was found to be positively associated with depression. In contrast, having an emotionally supportive family was found to be negatively associated with depression. Congruent with the Self-Medication Hypothesis, depression was found to be positively associated with impaired control over drinking. Physical neglect was found to be positively associated with impaired control. Lastly, emotional abuse was found to be indirectly linked to increased heavy episodic drinking and alcohol-related problems through depression and impaired control.
ContributorsBobel, Emily Rebecca Leslie (Author) / Patock-Peckham, Julie (Thesis director) / Glenberg, Arthur (Committee member) / Karoly, Paul (Committee member) / Department of Psychology (Contributor) / School of Criminology and Criminal Justice (Contributor) / Barrett, The Honors College (Contributor)
Created2018-12
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
Polysubstance abuse is far more common than single substance abuse. One of the most widely abused, yet greatly understudied combination of drugs is the simultaneous use of methamphetamine (meth) and alcohol. Because little research has been conducted on the co-abuse of meth and alcohol, it is important to study the behavioral and neural mechanisms underlying the use of both to combat addiction and come closer to finding an effective treatment of this form of drug abuse. This study uses a rodent model to attempt to identify the mechanisms underlying this co-abuse through the stimulation of the medial forebrain bundle (MFB) and thus the activation of the mesocorticolimbic pathway, the brain's pleasure circuit. First, self-stimulation thresholds (the lowest electrical current the rats are willing to respond for) were determined using a process called Discrete Trials Training. This threshold was later used as a baseline measure to reference when the rats were administered the drugs of abuse: meth and alcohol, both alone and in combination. Our overall results did not show any significant effects of combining alcohol and meth relative to the effects of either drug alone, although subject attrition may have resulted in sample sizes that were statistically underpowered. The results of this and future studies will help provide a clearer understanding of the neural mechanisms underlying the polyabuse of meth and alcohol and can potentially lead to more successfully combating and treating this addiction.
ContributorsDrafton, Kaitlyn Marie (Author) / Olive, Foster (Thesis director) / Glenberg, Arthur (Committee member) / Sanford School of Social and Family Dynamics (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
Description
This project investigated how alcohol might affect rates of Intimate Partner Aggression (IPA) within Hispanic populations specifically. Hispanics have the highest rates of IPA broadly speaking in the U.S., and I decided that further insight could be gleaned on why this might be by looking into how alcohol consumption might affect these rates. Data were gathered from Project IDEA, the research fellowship which this thesis piggybacked off of. Project IDEA was a survey asking couples about their drinking habits and relationship dynamics for the purpose of collecting more data on the connection between alcohol and IPA. My thesis focused more specifically on the Hispanic members of the sample. Ultimately, I found that Hispanics tend to engage in more heavy episodic drinking (i.e., drinking more in one sitting) than non-Hispanics, that heavy episodic drinking was positively correlated with IPA, and that Hispanics engaged more in all forms of IPA except for psychological perpetration than non-Hispanics. This essentially tells me that heavy episodic drinking might have something to do with the higher rates of IPA in Hispanic populations, but there is no definite causal relationship, and more research has to be done in this area.
ContributorsAcosta Huerta, Marcos (Author) / Davis, Kelly (Thesis director) / Hammett, Julia (Committee member) / Barrett, The Honors College (Contributor) / School of Criminology and Criminal Justice (Contributor) / Department of Psychology (Contributor)
Created2023-05