Professional Education

  • Doctor of Philosophy, Baylor College Of Medicine (2019)

Stanford Advisors

Contact

  • Academic
    tstay@stanford.edu
    University - Scholar Department: Neurobiology Position: Postdoctoral Scholar
    • D250B Fairchild Science Building
    • 299 Campus Drive West
    • Stanford University
    • Stanford,  California  94305-5125 

Additional Info

  • Mail Code: 5125

Current Research and Scholarly Interests

I am investigating the sensory pathways that contribute to establishing the highly conserved vestibulo-ocular reflex, and how they modify the reflex through learning. This complements my previous studies of the uvula-nodulus by examining dynamic adaptations in flocculus, the other half of the traditional vestibulo-cerebellum. I will be using simultaneous population recordings from multiple nodes in the vestibular circuit while providing diverse behavioral stimuli, then using general linear modeling to infer the relative impact of predictor variables on response variables. Additionally, I will use genetic tools to perturb elements of the signaling pathways to examine their respective role in establishing both the temporal filtering done by target neurons as well as gain and phase adaptation.

All Publications

  • In vivo cerebellar circuit function is disrupted in an mdx mouse model of Duchenne muscular dystrophy DISEASE MODELS & MECHANISMS Stay, T. L., Miterko, L. N., Arancillo, M., Lin, T., Sillitoe, R. 2020; 13 (2)

    Abstract

    Duchenne muscular dystrophy (DMD) is a debilitating and ultimately lethal disease involving progressive muscle degeneration and neurological dysfunction. DMD is caused by mutations in the dystrophin gene, which result in extremely low or total loss of dystrophin protein expression. In the brain, dystrophin is heavily localized to cerebellar Purkinje cells, which control motor and non-motor functions. In vitro experiments in mouse Purkinje cells revealed that loss of dystrophin leads to low firing rates and high spiking variability. However, it is still unclear how the loss of dystrophin affects cerebellar function in the intact brain. Here, we used in vivo electrophysiology to record Purkinje cells and cerebellar nuclear neurons in awake and anesthetized female mdx (also known as Dmd) mice. Purkinje cell simple spike firing rate is significantly lower in mdx mice compared to controls. Although simple spike firing regularity is not affected, complex spike regularity is increased in mdx mutants. Mean firing rate in cerebellar nuclear neurons is not altered in mdx mice, but their local firing pattern is irregular. Based on the relatively well-preserved cytoarchitecture in the mdx cerebellum, our data suggest that faulty signals across the circuit between Purkinje cells and cerebellar nuclei drive the abnormal firing activity. The in vivo requirements of dystrophin during cerebellar circuit communication could help explain the motor and cognitive anomalies seen in individuals with DMD.This article has an associated First Person interview with the first author of the paper.

    View details for DOI 10.1242/dmm.040840

    View details for Web of Science ID 000518475500004

    View details for PubMedID 31704708

    View details for PubMedCentralID PMC6906634

  • First person - Trace Stay DISEASE MODELS & MECHANISMS Stay, T. 2020; 13 (2)

    View details for DOI 10.1242/dmm.043356

    View details for Web of Science ID 000518475500020