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  • Undergraduate Poster Abstracts
  • Neuroscience

    FRI-G33 LONG-TERM FOLLOW-UP OF CAROTID ARTERY BLISTER ANEURYSMS

    • Mason Brown ;
    • Cris Guandique ;
    • Johnathan Parish ;
    • Michael Tu ;
    • Richard Kim ;
    • Bradley Bohnstedt ;
    • Aaron Cohen-Gadol ;

    FRI-G33

    LONG-TERM FOLLOW-UP OF CAROTID ARTERY BLISTER ANEURYSMS

    Mason Brown, Cris Guandique, Johnathan Parish, Michael Tu, Richard Kim, Bradley Bohnstedt, Aaron Cohen-Gadol.

    Goodman Campbell Brain and Spine, Indiana University School of Medicine, Indianapolis, IN.

    This study looks to address the long-term outcome for patients treated for blister aneurysms of non-branching sites of the internal carotid artery. Twenty two patients were treated for 29 blister aneurysms of the ICA out of 49 total aneurysms. Four patients did not survive treatment and were further excluded from the study. Ten patients (55.6%) had multiple aneurysms. Eleven patients (61.1%) presented with aneurysmal subarachnoid hemorrhage. The mean admission Hunt and Hess score was 1.6. Twelve patients (67%) were initially treated using microsurgical direct clipping and 6 patients (33%) with endovascular coiling. Of those treated microsurgically, 5 patients showed evidence of recurrence on follow up imaging and were treated surgically with reclipping. Of the 6 patients initially treated with coiling, 1 patient showed evidence of recurrence and was retreated with endovascular coil. There was 1 case with intraoperative rupture with direct clipping, and no cases of postoperative rebleed. Follow up imaging was available for 9 patients with a mean follow up of 4.2 ± 3.1 years. This study features the largest cohort and longest followup of patients with blister aneurysms at non-branching sites of the internal carotid artery. Although there is much disagreement on the optimal treatment for blister aneurysms, we present evidence that either direct surgical clip ligation or endovascular treatment as sufficient for good long term outcome. Due to the severity and outcome of this rare disease, it is necessary to mandate clinical and angiographic followup and continue to explore new methods in the management of blister aneurysms.

    FRI-G34 SEX DIFFERENCES IN THE MICROGLIAL RESPONSES TO CEREBRAL ISCHEMIA

    • Monica M. Gaudier-Diaz ;
    • Ning Zhang ;
    • A. Courtney DeVries ;

    FRI-G34

    SEX DIFFERENCES IN THE MICROGLIAL RESPONSES TO CEREBRAL ISCHEMIA

    Monica M. Gaudier-Diaz, Ning Zhang, A. Courtney DeVries.

    The Ohio State University, Columbus, OH.

    Cerebral ischemia, caused by cardiac arrest and stroke, is a leading cause of death and disability worldwide. Thus, it is important to find ways to prevent it, facilitate recovery, and improve the quality of life of survivors. Social isolation increases neuroinflammation, neuronal death, and functional impairment following cerebral ischemia. We hypothesize that microglia, innate immune cells of the nervous system, modulate the detrimental effects of social isolation on ischemic outcome. Environmental stressors can sensitize microglia to respond in an exaggerated manner on further immune stimulation; it is plausible that social isolation does the same. To study the effects of social environment on the microglial response to cerebral ischemia, mice were pair-housed or socially isolated, and a week later exposed to cardiac arrest/cardiopulmonary resuscitation (CA/CPR) or the sham procedure. Brains were collected to measure microglial gene expression. Among individually housed male mice that received CA/CPR, there was increased microglial gene expression of proinflammatory cytokines IL-1β and IL-6 relative to sham controls; in contrast, gene expression among pair-housed males did not differ between CA/CPR and sham groups. This suggests that social isolation exacerbates ischemia-induced neuroinflammation through microglial production of proinflammatory cytokines. Nonetheless, in female mice there was increased microglial gene expression of proinflammatory cytokines following CA/CPR relative to sham regardless of housing. Additional studies are necessary to determine the mechanism underlying this sex difference on the effects of social environment on ischemia-induced neuroinflammation. In sum, social environment can have a substantial influence on the pathophysiological response to global cerebral ischemia.

    THU-G22 FUNCTIONAL SCREENS TO IDENTIFY NEURONS IN THE LARVAL BRAIN OF DROSOPHILA THAT CONTROL MOTOR PROGRAMS

    • Matthew Clark ;
    • Ellie Heckscher ;
    • Chris Doe ;

    THU-G22

    FUNCTIONAL SCREENS TO IDENTIFY NEURONS IN THE LARVAL BRAIN OF DROSOPHILA THAT CONTROL MOTOR PROGRAMS

    Matthew Clark, Ellie Heckscher, Chris Doe.

    University of Oregon, Eugene, OR.

    Drosophila larval locomotion is governed by patterns of connections and the activity of inhibitory and excitatory interneurons within the ventral nerve cord. These networks of connections influence the firing patterns of motor neurons that drive muscle contractions and larval locomotion. While the highly stereotyped anatomy of the neuromuscular system is well studied, the nature of the upstream interneuronal network remains poorly elucidated. Based on in vivo muscle contraction crawl patterns, previously described myotopy, and results from our behavior screen, we hypothesize that each putative motor unit has discrete interneuronal inputs that can control firing timing. Understanding interneuronal function is challenging due to their diversity and number within the ventral nerve cord with close to 300 neurons per hemisegment currently having an unknown function. Using the gain-of-function neuronal activation tool UAS-dTrpA1, we activated random subsets of neurons within the larval CNS using the GAL4/UAS system. On activation of UAS-dTrpA1 in small subsets of neurons (< 15 per hemisegment), we observed many unique behavioral phenotypes. We are currently working to classify these unique behavioral phenotypes, as well as fully characterizing their expression patterns.

    FRI-G22 THE HOMEODOMAIN PROTEINS SIX3 AND SIX6 ARE IMPORTANT IN THE DEVELOPMENT OF GNRH NEURONS IN MICE

    • Erica Pandolfi ;
    • Pamela Mellon ;

    FRI-G22

    THE HOMEODOMAIN PROTEINS SIX3 AND SIX6 ARE IMPORTANT IN THE DEVELOPMENT OF GNRH NEURONS IN MICE

    Erica Pandolfi, Pamela Mellon.

    University of California, San Diego, La Jolla, CA.

    A reduction in gonadotropin-releasing hormone (GnRH) neurons causes GnRH deficiency and infertility. GnRH neurons originate in the olfactory placode and migrate to the hypothalamus. Two genes that play a role in the development of these neurons are Six3 and Six6. However, the effect of Six3 on neuronal development has not yet been tested, and further exploration into the loss of GnRH neurons in the Six6KO mouse model must be conducted. The purpose of our work is to determine what role Six3 and Six6 play in the development of GnRH neurons and fertility. We hypothesize that Six3 and Six6 are essential regulators of GnRH neuronal development, and are important in the development of GnRH neurons. Mice with a specific deletion of Six3 from GnRH neurons were used, as well as Six6KO mice. Neuronal counting in Six3Flox/GnRHCre mice showed a 30% increase in GnRH neuron numbers in the embryo and adult. This 30% increase in GnRH neurons did not significantly impact fertility. In contrast, neuronal counting revealed that Six6KO mice first showed reduction in the number of GnRH neurons at E14.5. The balance of Six3 and Six6 in GnRH neurons is crucial for the correct maturation of GnRH neurons, and determines the number of GnRH neurons in the mouse, thus regulating fertility. Our findings support the hypothesis that the Six6 protein is an essential positive regulator of GnRH neuron survival; and that the Six3 protein functions as an inhibitor of GnRH neuron proliferation or survival.

    THU-G33 THE INVOLVEMENT OF PHOSPHATIDYLINOSITOL-3'-KINASE PATHWAY IN THE NEUROPROTECTIVE EFFECTS OF ASHWAGANDHA IN HIPPOCAMPAL NEURONS

    • Dahae Hwang ;
    • Amelia Russo-Neustadt ;
    • Michael Chen ;

    THU-G33

    THE INVOLVEMENT OF PHOSPHATIDYLINOSITOL-3'-KINASE PATHWAY IN THE NEUROPROTECTIVE EFFECTS OF ASHWAGANDHA IN HIPPOCAMPAL NEURONS

    Dahae Hwang, Amelia Russo-Neustadt, Michael Chen.

    California State University, Los Angeles, Los Angeles, CA.

    There is ample evidence that ashwagandha (Withania somniferum), also called Indian ginseng, has many beneficial effects such as neuroprotection and improved mental and cognitive health. Recent studies from our lab have shown that 2 active components of ashwaghanda, withania A and withaferin A, increase survival of hippocampal neurons that have been deprived of critical nutrients in culture. This effect may be mediated through activation of the phosphatidylinositol-3’-kinase (PI-3K) pathway, which is known to enhance cell survival. This pathway activates transcription factors such as CREB and BDNF, whose expression is a well-known marker of enhanced cell survival. We will test this hypothesis by administering a highly selective PI-3K inhibitor, LY294002, containing withania A and withaferin A with and without critical nutrients, to hippocampal neurons in culture. Cell survival will be monitored by the lactate dehydrogenase assay, and the activation of the PI-3K pathway will be evaluated via western blotting. We expect treatment with LY294002 will abolish hippocampal neuronal survival in the presence of withania A and withaferin A under nutrient depletion, thereby confirming our hypothesis. If the application of LY294002 has no effect, another pathway, such as mitogen-activated protein kinase (MAPK) will be explored. This study is significant because identifying the pathway that is involved in the effects of ashwagandha will help researchers develop potential therapeutic drugs for Alzheimer’s disease and neurological disorders involving neurodegeneration.