A single link to the first track to allow the export script to build the search page
  • Undergraduate Poster Abstracts
  • Neuroscience

    Room National Harbor 7

    ap037 ABERRANT ASTROCYTE MATURATION CONTRIBUTES TO RETT SYNDROME PATHOGENESIS

    • Natasha Pacheco ;
    • Leanne Holt ;
    • David Crossman ;
    • Michelle Olsen ;

    n/a

    ABERRANT ASTROCYTE MATURATION CONTRIBUTES TO RETT SYNDROME PATHOGENESIS

    Natasha Pacheco, Leanne Holt, David Crossman, Michelle Olsen.

    The University of Alabama at Birmingham, Birmingham, AL.

    Rett syndrome (RTT) is an x-linked neurodevelopmental disorder caused by mutations in the transcriptional regulator MeCP2. RTT is characterized by having apparently normal development until 6 to 18 months, when a progressive decline in motor and language functions begins and breathing abnormalities and seizures present. Astrocytes, the most abundant cell type in the central nervous system (CNS), have recently been shown to express MeCP2. Importantly, postnatal re-expression of MeCP2 in astrocytes in globally Mecp2-deficient mice ameliorated many RTT disease symptoms, indicating that deficiencies in astrocytic function contribute to the pathophysiology of RTT. However, the causative mechanisms are currently unknown. Given the broad transcriptional regulatory role of MeCP2, we predict that many astrocytic genes are dysregulated. To test this prediction, we have utilized RNA-Seq analysis to examine global gene expression changes in enriched cortical astrocytes compared to whole cortex tissue from symptomatic Mecp2-deficient mice compared to wild-type (WT) littermate controls. We have identified over 1,700 significant and differentially expressed genes in cortical astrocytes. Pathway analysis in our cortical astrocyte dataset has identified disrupted pathways involved in inflammation and metabolism as well as gastrointestinal, neurological, and immunological diseases. Furthermore, molecular and cellular functions associated with proper astrocytic maturation were also identified as being disrupted. Our current work is directed at understanding when in the disease process these changes occur. Through the identification of key groups of astrocytic genes, proteins, and pathways, we can begin to tease apart the mechanisms in which astrocytes contribute to RTT pathogenesis, possibly identifying new and much needed therapeutic targets for RTT patients.

    ap038 IDENTIFYING NEURONAL DYNAMICS OF SHORT-TERM ASSOCIATIVE MEMORY IN C. ELEGANS

    • Angelina Sylvain ;
    • Mohammad Rahimi ;
    • Geneva Stein ;
    • Coleen Murphy ;

    n/a

    IDENTIFYING NEURONAL DYNAMICS OF SHORT-TERM ASSOCIATIVE MEMORY IN C. ELEGANS

    Angelina Sylvain1, Mohammad Rahimi2, Geneva Stein3, Coleen Murphy2.

    1Princeton Neuroscience Institute, Princeton University, Princeton, NJ, 2Lewis Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, 3Princeton University, Princeton, NJ.

    All animals make decisions based on the information they learn and remember about their environment, which requires neural plasticity. C. elegans is able to remember an association between food and odor (butanone) for a short time (less than 2 hours), an ability that is equivalent to classical short-term associative memory (STAM). We have defined many of the molecular components of this process through genetic analyses, but the circuit dynamics of STAM are not yet known. We have found that AWCon exhibits increased odor-evoked Ca2+ responses upon STAM training, and that the number of animals responsive to the odorant decreases with increased post-conditioning time in close parallel to that observed in population STAM assays. We developed a novel microfluidic chip to simultaneously assay AWCon activity and animal behavior to test whether the enhanced neuronal response correlates with the behavioral changes, and have identified neurons required for STAM performance. Finally, we have used these tools to begin to address the mechanism underlying daf-2's 3-fold increased STAM duration. These studies provide the framework for comprehensively understanding molecular and neural circuit mechanisms of short-term associative memory. 

    ap039 AGE-DEPENDENT ION CHANNEL STABILITY IN NEURONS

    • Maximiliano Vallejos ;
    • Susan Tsunoda ;

    n/a

    AGE-DEPENDENT ION CHANNEL STABILITY IN NEURONS

    Maximiliano Vallejos, Susan Tsunoda.

    Colorado State University, Fort Collins, CO.

    Aging typically relates to a decline in cognitive abilities and coordinated behaviors. These changes are likely due to age-related changes in neuronal signaling. Ion channels, which underlie much of neuronal signaling, have been described to undergo age-dependent changes in aggregation and distribution. Little is known about the aging effects on ion channel stability. Here, we show an age-dependent decrease in Shal/Kv4 ion channel in Drosophila. Shal is a voltage-gated potassium channel involved in locomotion, learning, and memory. We report that natural age-dependent decline in locomotion is improved by Shal overexpression. To investigate the mechanisms underlying the age-dependent decline in Shal protein, we quantitated Shal mRNA in young/old flies. Shal mRNA levels remain unaffected, suggesting that transcription is not involved in declining Shal protein. To test if the decline involves loss of a scaffolding protein, we examined SIDL (Shal-interactor of di-leucine), a novel protein identified to interact with a highly conserved C-terminal di-leucine motif required for somato-dendritic targeting. We found that SIDL transcript is significantly decreased with age. To test whether SIDL is necessary for Shal stability, we used an RNAi-SIDL construct resulting in 60% and 25% SIDL mRNA knockdown at larval and adult stages, respectively. This knockdown resulted in a 40% decrease of Shal protein levels in adults, suggesting that SIDL is required for Shal stability in vivo. Interestingly, RNAi-SIDL expressed during development resulted in decreased Drosophila viability. Our results suggest that loss of SIDL during aging leads to a decline in Shal and deterioration in behaviors such as locomotion.

    ap040 MAGNETOENCEPHALOGRAPHY STUDY ON MULTISENSORY INTEGRATION IN ADOLESCENTS WITH FETAL ALCOHOL SPECTRUM DISORDER

    • Alfredo Bolanos ;
    • Brian Coffman ;
    • John Pinner ;
    • Piyadasa Kodituwakku ;
    • Julia Stephen ;

    n/a

    MAGNETOENCEPHALOGRAPHY STUDY ON MULTISENSORY INTEGRATION IN ADOLESCENTS WITH FETAL ALCOHOL SPECTRUM DISORDER

    Alfredo Bolanos1, Brian Coffman2, John Pinner1, Piyadasa Kodituwakku1, Julia Stephen1.

    1The University of New Mexico, Albuquerque, NM, 2The Mind Research Network, Albuquerque, NM.

    It is now known that children exposed to substantial amounts of alcohol in utero display a broad range of cognitive and behavioral deficits along with functional and structural neural anomalies. Previous studies have shown impairments in sensory processing and executive functioning, suggesting atypical brain development in children with fetal alcohol spectrum disorder (FASD). To further our knowledge of sensory processing in children with FASD, brain responses were recorded using magnetoencephalography (MEG) from 19 adolescents with FASD and 23 age-matched, typically developing controls during a cross-hemisphere multisensory paradigm with passive auditory, somatosensory, and multisensory stimulation. We hypothesized that neural oscillations would be altered in adolescents with FASD. Time-frequency analysis of the MEG data revealed a significant decrease in oscillatory power for 6 conditions in the FASD group based on permutation testing of significant group differences. Through one-sample t-tests, we noted that between-group differences in multisensory conditions were accompanied by a significant within-group increase in oscillatory power relative to baseline in the control group and a decrease in the FASD group. Furthermore, results revealed that unisensory oscillatory power predicted multisensory oscillatory power more strongly in the control group than in the FASD group. Yet, oscillatory power only correlated with attention and impulsivity scores in the FASD group. The present results provide further evidence of abnormal gamma-band oscillations in adolescents with FASD when responding to sensory stimuli, which may be associated with the neurobehavioral deficits experienced by individuals with FASD by restricting their ability to respond properly to external stimuli during day-to-day interactions.