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- All Subjects: Psychiatry
- Creators: Benoit, Renee
- Creators: Edson, Belle
- Creators: Hruschka, Daniel
- Member of: Theses and Dissertations
Description
Environmental and genetic factors contribute to schizophrenia etiology, yet few studies have demonstrated how environmental stimuli impact genes associated with the disorder. Immediate early genes (IEGs) are of great interest to schizophrenia research because they are activated in response to physiological stress from the environment, and subsequently regulate the expression of downstream genes that are essential to neuropsychiatric function. An IEG, early growth response 3 (EGR3) has been identified as a main gene involved in a network of transcription factors implicated in schizophrenia susceptibility. The serotonin 2A receptor (5-HT2AR) seems to play an important role in schizophrenia and the dysfunction of the 5-HT2AR encoding gene, HTR2A, within the prefrontal cortex (PFC) contributes to multiple psychiatric illnesses including schizophrenia. EGR3's role as a transcription factor that is activated by environmental stimuli suggests it may regulate Htr2a transcription in response to physiological stress, thus affecting 5-HT2AR function in the prefrontal cortex (PFC). The aim of this study was to examine the relationship between Egr3 activation and Htr2a expression after an environmental stimulus. Sleep deprivation is an acute physiological stressor that activates Egr3. Therefore to examine the relationship between Egr3 and Htr2a expression after an acute stress, wild type and Egr3 knockout mice that express EGFP under the control of the Htr2a promoter were sleep deprived for 8 hours. We used immunohistochemistry to determine the location and density of Htr2a-EGFP expression after sleep deprivation and found that Htr2a-EGFP expression was not affected by sex or subregions of the PFC. Additionally, Htr2a-EGFP expression was not affected by the loss of Egr3 or sleep deprivation within the PFC. The LPFC subregions, layers V and VI showed significantly more Htr2a-EGFP expression than layers I-III in all animals for both sleep deprivation and control conditions. Possible explanations for the lack of significant effects in this study may be the limited sample size or possible biological abnormalities in the Htr2a-EGFP mice. Nonetheless, we did successfully visualize the anatomical distribution of Htr2a in the prefrontal cortex via immunohistochemical staining. This study and future studies will provide insight into how Egr3 activation affects Htr2a expression in the PFC and how physiological stress from the environment can alter candidate schizophrenia gene function.
ContributorsSabatino, Alissa Marie (Author) / Gallitano, Amelia (Thesis director) / Hruschka, Daniel (Thesis director) / Maple, Amanda (Committee member) / Barrett, The Honors College (Contributor)
Created2014-05
Description
The American Psychiatric Association's Diagnostic and Statistical Manual, the official guidebook to psychiatric diagnosis in America, currently exempts the recently bereaved from being diagnosed with depression unless their experiences are marked by feelings of extreme worthlessness, significant functional impairment, psychotic symptoms, psychomotor retardation, or suicidal ideation. Ordinary symptoms of depression, such as sleeplessness or loss of appetite, are considered healthy, functional emotional responses to the loss of a loved one. The bereavement exemption is slated for removal in the upcoming fifth edition of the Diagnostic and Statistical Manual, functionally redefining the emotional distress of bereavement as a psychiatric disorder. This study employs genealogical analysis to expose the multiplicity of forces that shape modern psychiatry and the ways that the redefinition of depression functions strategically in the social negotiation of truth and power. Under the guise of etiological and prescriptive neutrality, the redefinition of depression promotes a deeply biological model of psychiatric disorder, a medicalized understanding of human emotion, and a pharmacological approach to the treatment of emotional distress. Through genealogical analysis, this project seeks to enable informed, meaningful ethico-political responses to these developments.
ContributorsMeeth, John (Author) / Edson, Belle (Thesis advisor) / Palazzolo, Kellie (Thesis advisor) / Quinlivan, Raena (Committee member) / Arizona State University (Publisher)
Created2011
Description
Pediatric anxiety disorders are highly prevalent and while pharmacological intervention seems to be an effective treatment, the validity of reported adverse side effects remains unclear. <br/><br/>Objective: To analyze the nature of evidence regarding adverse side effects in the pharmacological treatment of pediatric anxiety disorders. <br/><br/>Approach: A search using Google Scholar, PubMed, and PsychInfo was conducted for meta-analyses of pharmacological treatment of pediatric anxiety disorders as well as randomized controlled trials. The focus was on adverse events.<br/><br/>Results and Conclusion: Reportings of a limited number of adverse events were found among resources available to clinician and patient informed sources to inform pharmacological treatment of pediatric anxiety disorders. Only a small fraction of adverse side effects were found in the research literature. This finding raises concerns about making informed decisions to treat pediatric anxiety disorders with pharmacotherapy.
ContributorsMartin, Mark (Co-author) / Reyes, Trevin (Co-author) / Whooley, Max (Co-author) / Pina, Armando (Thesis director) / Benoit, Renee (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2021-05