About

Court Alan Hull is involved in research related to the role of cell-type specific circuits for inhibition and disinhibition in cerebellar learning and behavior. His work is supported by a grant from Duke Scholars, administered by the Neurobiology department, and funded by the National Institute of Neurological Disorders and Stroke. The project started on August 1, 2025, and is scheduled to end on April 30, 2030. Further details about his background, research contributions, or professional history are not provided in the page text.

Research topics

• Neuroscience
• Computer Science
• Machine Learning
• Biology
• Artificial Intelligence
• Psychology
• Medicine
• Physics
• Biochemistry
• Cognitive science
• Cell biology
• Chemistry

Selected publications

• Consensus Paper: Models of Cerebellar Functions

  The Cerebellum · 2026-02-09 · 2 citations

  articleOpen access

  For a long time, from the nineteenth century to most of the twentieth century, the cerebellum was thought to be an organ that regulates movement. Towards the end of the twentieth century, the brain functions associated with the cerebellum began to extend beyond motor control. Now, there is a consensus that the cerebellum is involved not only in motor functions but also in the most basic autonomic functions and the most complex cognitive and emotional functions, with a focus on predictions and internal models. A new functional model of the cerebellum is needed to explain all layers of brain functions by extending predictive computations in the cerebellum. On the other hand, the cerebellum and the basal ganglia were believed to be independent and complementary motor centers that lacked direct neural connections. For example, in neurophysiology classes in the 1980s, the characteristics of cerebellar ataxia were summarized as hyperkinetic and hypotonia, while the characteristics of Parkinson's disease (traditionally classified as "basal ganglia disorder") were summarized as hypokinetic and hypertonia, and therefore their functions were assumed at opposite poles, without interactions between the two main subcortical systems. The cerebellum and the basal ganglia were also assigned contrasting models regarding their learning mechanisms. Namely, the cerebellum was assumed to employ supervised learning with error signals, while the basal ganglia were assumed to employ reinforcement learning with reward prediction errors. However, recent neuroanatomical studies have demonstrated a number of novel connections between them, questioning their independence. Moreover, recent single-neuron recording and inactivation studies provided evidence that the cerebellum may also be involved in reinforcement learning. The cerebellum is neither independent of the basal ganglia nor exclusively specialized for supervised learning. We now need a new, general model to explain the contradiction between the known uniformity of the cerebellar cortex's structure and the newly added diversity of brain functions to which the cerebellum contributes. This consensus paper summarizes many of the seeds of such a new theory. The panel of experts (1) highlights the importance of the anatomical connectivity between cerebellar circuitry and basal ganglia, (2) points out that the anatomy of the cerebellum is unique and allows predictive computations in motor and extra-motor domains such as cognition, affect, social interactions and reward processes, (3) underlines the need to further elucidate the nature of interactions between cerebellar cortex and cerebellar nuclei to better understand cerebellar and psychiatric disorders and (4) suggests that common operations may underlie the motor and non-motor functions of the cerebellar circuitry. Cerebellar models remain a major topic of research to improve our understanding of the numerous cerebellar activities and to better understand the complexity of cerebellar disorders.

  PublisherOA PDFDOI

• Climbing fibres recruit disinhibition to enhance Purkinje cell calcium signals

  Nature · 2026-03-18 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• ASTN2 in ASD and neurodevelopmental disorders

  Current topics in developmental biology/Current Topics in Developmental Biology · 2026-01-01

  book-chapter
  PublisherDOI

• Data for: Climbing fibres recruit disinhibition to enhance Purkinje cell Ca2+ signals

  Harvard Dataverse · 2026-02-24

  datasetOpen access

  Data for: Climbing fibres recruit disinhibition to enhance Purkinje cell Ca2+ signals, Nature (2026). The EM dataset is deposited at the BossDB repository (https://bossdb.org/project/nguyen_thomas2022).

  PublisherDOI

• Climbing fibers recruit disinhibition to enhance Purkinje cell Ca2+ signals

  Figshare · 2026-03-19

  datasetOpen accessSenior author

  Data corresponding to indicated figures in Climbing fibers recruit disinhibition to enhance Purkinje cell Ca2+ signals

  PublisherDOI

• Climbing fibers recruit disinhibition to enhance Purkinje cell Ca2+ signals

  Figshare · 2026-03-19

  datasetOpen accessSenior author

  Data corresponding to indicated figures in Climbing fibers recruit disinhibition to enhance Purkinje cell Ca2+ signals

  PublisherDOI

• Reward-driven cerebellar climbing fiber activity influences both neural and behavioral learning

  Current Biology · 2025-08-22 · 2 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• A deep learning strategy to identify cell types across species from high-density extracellular recordings

  Cell · 2025-02-28 · 29 citations

  articleOpen access
  PublisherOA PDFDOI

• Structural and functional evidence for ephaptic control of Purkinje cell spike timing by networks of molecular layer interneurons

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-12-29

  articleOpen access

  Abstract Axon collaterals of type 1 molecular layer interneurons (MLI1s) contribute to pinceaux that engulf the initial segments of Purkinje cell (PC) axons and generate extracellular signals that ephaptically inhibit PCs. Here we show that a remarkably large number of MLI1s (∼50) contribute to each pinceau, and that this allows networks of synchronously firing MLI1s to use ephaptic signals to control the precise timing of PC firing in vivo .

  PublisherOA PDFDOI

• Climbing fibers selectively recruit disinhibitory interneurons to enhance dendritic calcium signaling in cerebellar Purkinje cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-23 · 2 citations

  preprintOpen access

  Abstract Climbing fiber (CF) inputs to Purkinje cells (PCs) instruct plasticity and learning in the cerebellum 1–3 . Paradoxically, CFs also excite molecular layer interneurons (MLIs) 4,5 , a cell-type that inhibits PCs and can restrict plasticity and learning 6,7 . However, two types of MLIs with opposing influences have recently been identified: MLI1s inhibit PCs, reduce dendritic calcium signals, and suppress plasticity of granule cell to PC synapses 2,6–9 , whereas MLI2s inhibit MLI1s and disinhibit PCs 8 . To determine how CFs can activate MLIs without also suppressing the PC calcium signals necessary for plasticity and learning, we investigated the specificity of CF inputs onto MLIs. Serial EM reconstructions indicate that CFs contact both MLI subtypes without making conventional synapses, but more CFs contact each MLI2 via more sites with larger contact areas. Slice experiments indicate that CFs preferentially excite MLI2s via glutamate spillover 4,5 . In agreement with these anatomical and slice experiments, in vivo Neuropixels recordings show that spontaneous CF activity excites MLI2s, inhibits MLI1s, and disinhibits PCs. In contrast, learning-related sensory stimulation produced more complex responses, driving convergent CF and granule cell inputs that could either activate or suppress MLI1s. This balance was robustly shifted toward MLI1 suppression when CFs were synchronously active, in turn elevating the PC dendritic calcium signals necessary for LTD. These data provide mechanistic insight into why CF synchrony can be highly effective at inducing cerebellar learning 2,3 by revealing a critical disinhibitory circuit that allows CFs to act through MLIs to enhance PC dendritic calcium signals necessary for plasticity.

  PublisherDOI

Recent grants

• NIH Grant F32NS060585

  NIH · $96k · 2009

• Neuromodulatory Control of Cerebellar Synaptic Processing and Sensory Input

  NIH · $1.7M · 2016–2021

• NIH Grant F31NS042506

  NIH · $98k · 2005

• Canonical computations for motor learning by the cerebellar cortex micro-circuit

  NIH · $6.4M · 2019–2024

Frequent coauthors

• Henrique von Gersdorff

  Vollum Institute

  22 shared

• N.A. Buchwald

  13 shared

• Luke C. Bartelt

  University of California, Irvine

  9 shared

• G.F. Heuser

  University of Siegen

  9 shared

• Everett J. Wyers

  State University of New York

  9 shared

• Wade G. Regehr

  Harvard University

  9 shared

• Lj. Rakić

  Univerzitetski Klinički Centar Srbije

  9 shared

• Massimo Scanziani

  University of California, San Francisco

  7 shared

Labs

• Hull LabPI

Education

• PhD

  Vollum Institute

  2005

• BS Biology

  University of Puget Sound

  1999