About

Kathleen E. Cullen is the Principal Investigator at the Cullen Lab. She holds a B. Sc. in Neuroscience and a B. A. in Bioengineering from Brown University. She earned her Ph.D. from the Committee on Neurobiology (Behavioural Neurophysiology) at the University of Chicago. Following her doctoral studies, she completed a postdoctoral fellowship in the Department of Neurology and Neurosurgery at the Montreal Neurological Institute. Her academic and research career is focused on neuroscience, with a specialization in neurophysiology and biomedical engineering. She leads research efforts at Johns Hopkins University, where she is involved in advancing the understanding of neural mechanisms and their applications in biomedical engineering.

Research topics

• Computer Science
• Neuroscience
• Biology
• Biochemistry
• Psychology
• Cell biology
• Physics
• Anatomy

Selected publications

• Effects of Electrode Position on Vestibular Implant Performance in Rhesus Macaque

  Journal of the Association for Research in Otolaryngology · 2026-01-14

  articleOpen access
  PublisherOA PDFDOI

• SCREWx: A Screwless, Chronic, Recoverable, and Lightweight Neuropixels fixture for freely-moving rodents

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-06

  articleOpen access

  Summary High-density Neuropixels probes enable the study of large neural populations with single-cell and sub-millisecond resolution. While single-probe and acute head-fixed experiments have yielded critical scientific insights, understanding the neural mechanisms underlying many complex behaviors requires simultaneous multi-region recordings in freely moving, chronically implanted animals. Various probe fixtures have been developed to enable high-density recording, but existing designs impose critical limitations: their substantial weight restricts the maximum probe count that smaller animals can support, their bulky dimensions constrain the proximity of targeted brain regions, and their complex assembly risks damaging the probe during insertion and recovery. In this paper, we present a lightweight, fully 3D-printable, compact, and screwless fixture for chronic Neuropixels implants in freely moving rodents that features simple mechanisms for stable implantation and safe extraction. Our fixture design enables stable, high-yield single-unit recordings for months-long experiments, along with an 83% successful probe extraction rate. This fixture design provides a robust and accessible solution for long-term, multi-probe chronic Neuropixels recordings, increasing experimental throughput and enabling more complex experimental designs to investigate brain-wide neural dynamics.

  PublisherOA PDFDOI

• Partitioning Neural Co-Variability

  PubMed Central · 2026-05-07

  preprintOpen access

  Trial-to-trial variability of neural responses has been linked to important aspects of neural computation and is essential for understanding how neuronal populations respond. While current overdispersion models treat each neuron's gain as independent of each other, this assumption fails to capture the network statistics of neuronal populations. As no existing model can capture overdispersed structured spiking gain-modulation across a neural population, network-level gain covariance remains largely unstudied. We thus present the Poisson matrix-normal latent variable (PMNLV) model, which extends single-neuron overdispersion to neural populations by placing a matrix-normal prior over the latent gain with a Kronecker-factored covariance. Spike counts are Poisson-distributed with a rate equal to the sum of a per-neuron stimulus tuning term and a matrix-normal gain, passed through a quadratic soft-rectifying link. We derive two complementary estimation algorithms: a variational EM (VEM) with a matrix-normal posterior that recovers dense Kronecker factors without structural assumptions, and a Kernel Tournament Method (KTM) that performs data-driven selection over a biologically motivated kernel dictionary and composite likelihood. On simulated data, both algorithms recover the inter-neuron and temporal covariance factors and accurate tuning curves. Applying VEM to Neuropixel recordings across four cortical regions of mouse visual hierarchy, we replicate a previous finding that single-neuron marginal variability changes little across cortical areas. We then show that shared population co-variability, invisible to scalar summaries e.g., the Fano factor, peaks in primary visual cortex and declines in higher visual areas. The PMNLV framework is applicable to any simultaneously recorded population where structured gain covariance is of scientific interest.

  PublisherDOI

• Eye-head coordination during goal-directed orienting in mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-01

  articleOpen accessSenior author

  In afoveate species such as mice, it is accepted that gaze is typically redirected by head movements with a saccade-and-fixate strategy, while the eyes primarily stabilize vision within a limited oculomotor range. This view suggests that the accompanying eye movements are primarily reflexive, driven by mechanisms like the vestibulo-ocular reflex (VOR). However, emerging evidence challenges this assumption, suggesting that eye movements during active head motion may not be purely reflex-driven. Here, we directly test whether eye movements in mice are actively coordinated as part of voluntary gaze redirection rather than being reflexive. By systematically monitoring head and pupil positions during goal-directed orienting in a cohort of male mice, we find that mice generated active saccadic eye movements whose onsets are tightly linked to head movements. Furthermore, these saccadic eye movements occur at markedly shorter latencies than reflexive quick-phase eye movements evoked by comparable passive head rotations. Importantly, the interplay between coordinated eye and head movements during voluntary orienting resemble the predictable, stereotyped gaze patterns seen in foveate animals, such as primates. Our results suggest that mice possess an evolutionarily conserved mechanism for gaze redirection, integrating voluntary eye-head coordination similar to that of foveate vertebrates. These findings reframe the prevailing view by demonstrating an actively coordinated eye-head component to gaze redirection under goal-directed conditions in mice, complementing established reflexive mechanisms.

  PublisherDOI

• Bat eye movements resolve a long-standing question in gaze control

  Current Biology · 2026-03-31 · 1 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Bat eye movements resolve a long-standing question in gaze control

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-12

  articleOpen accessSenior authorCorresponding

  Summary Eye movements enable visual information gathering and stabilize gaze via optokinetic (OKR) and vestibulo-ocular reflex (VOR) pathways. 1 Echolocating bats, despite their rapid and agile flight maneuvers to land upside down and navigate 3D space, have long been thought not to move their eyes, an assumption originating from Walls’s influential assertion over 80 years ago 2 but never tested with empirical measurements. Here we present quantitative analysis of eye movements driven by visual and vestibular signals in Seba’s short-tailed bat ( Carollia perspicillata ). Bats generated robust visually driven OKR with an oculomotor range of ∼±10°, and displayed strong otolith-mediated responses during off-vertical axis rotation. In contrast, they showed minimal semicircular canal–driven angular VOR (aVOR) for passive head rotations that elicit large, sustained responses in mice. Micro-CT reconstructions revealed that bats and mice have similar semicircular canal geometry, indicating that the weak aVOR does not reflect peripheral anatomical constraints. These findings provide the first empirical demonstration that bats make robust eye movements and exhibit strong visual and otolith-driven components of gaze stabilization. We propose that semicircular canal signals may be more strongly engaged during active flight and modulated by behavioral state–dependent tuning of vestibular pathways to support ecologically specialized behaviors.

  PublisherOA PDFDOI

• GPR156 is required in sensory hair cells for proper auditory and vestibular function

  Scientific Reports · 2026-01-17 · 2 citations

  articleOpen access

  Proper orientation of the apical cytoskeleton in auditory and vestibular hair cells is essential for their sensory function. A recently identified regulator of hair cell orientation is the G protein-coupled receptor GPR156, which signals through inhibitory heterotrimeric G proteins. In hair cells expressing the transcription factor EMX2, GPR156 is apically enriched and polarized at cell junctions. There, GPR156 signaling reverses the interpretation of tissue-level core planar cell polarity cues, effectively reversing the orientation of Emx2-positive compared to Emx2-negative hair cells. This mechanism establishes key anatomical features, such as the correct alignment of auditory outer hair cells and the line of polarity reversal in the otolith organs of the vestibular system. Null mice with constitutive Gpr156 inactivation exhibit severe hearing loss, mirroring congenital hearing impairment in human patients with homozygous GPR156 variants. These null mutants also display impaired swimming and vestibulo-ocular reflexes, although the nature of these vestibular deficits differs from those reported in Emx2 mutants. Here, to determine the extent to which functional deficits arise from hair cell misorientation, we conditionally inactivated Gpr156 in postmitotic hair cells in the inner ear. This targeted deletion approach recapitulated the misorientation phenotype observed in null mutants. Notably, 30–40% of cochlear and utricular hair cells affected in the null background retained normal orientation in conditional mutants, likely due to the later timing of Gpr156 inactivation. Despite reduced efficiency, conditional mutants exhibited similar, albeit predictably milder, auditory and vestibular dysfunction. As hair cells can carry out mechano-electrical transduction without GPR156, we conclude that sensory deficits mainly result from its essential role in hair cell orientation.

  PublisherDOI

• Acceleration and Velocity Dissociate Temporal Phases of Postural Control in Rhesus Macaques

  Journal of Neuroscience · 2026-03-30

  articleOpen accessSenior author

  Maintaining balance requires the nervous system to transform sensory signals about unexpected postural perturbations into precisely timed motor commands. Although human studies have established that postural responses unfold in distinct temporal phases, how specific kinematic variables structure these phases during rotational perturbations remains unresolved, because angular acceleration and velocity are typically confounded. Here, we developed a rhesus macaque model of postural control that independently manipulates angular acceleration and peak velocity during transient pitch and roll tilts in monkeys of either sex. By simultaneously measuring head kinematics—directly relevant to vestibular signaling—and center-of-pressure dynamics, we quantified how sensory inputs and motor outputs evolve across successive phases of the postural response. We show that short-latency postural responses (<100 ms) are primarily governed by angular acceleration, whereas medium-latency responses (100–200 ms) scale with angular velocity. This dissociation was robust across perturbation axes and accompanied by axis-dependent control strategies: roll tilts elicited constrained head motion consistent with active stabilization in space, whereas pitch tilts produced more compliant, platform-following behavior. Together, these findings identify distinct kinematic variables governing successive phases of balance control and establish a primate framework for linking neural circuit activity to the temporal organization of postural responses. Significance Statement Maintaining balance requires transforming sensory signals about unexpected body motion into precisely timed motor commands. Progress in understanding this process has been limited because angular acceleration and velocity are inherently coupled during rotational perturbations. Here, using a rhesus macaque model, we dissociate these kinematic variables and show that they govern distinct temporal phases of postural control: angular acceleration determines short-latency (<100 ms) responses, whereas angular velocity shapes medium-latency (100–200 ms) adjustments. We further demonstrate axis-dependent postural strategies that parallel those observed in humans. Together, these findings resolve a longstanding confound in balance research and establish a primate framework that will enable future studies to link neural circuit activity to the biomechanics of postural control.

  PublisherOA PDFDOI

• Acceleration and Velocity Dissociate Temporal Phases of Postural Control in Rhesus Macaques

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-21

  articleOpen accessSenior authorCorresponding

  Abstract Maintaining balance requires the nervous system to transform sensory signals about unexpected postural perturbations into precisely timed motor commands. Although human studies have established that postural responses unfold in distinct temporal phases, how specific kinematic variables structure these phases during rotational perturbations remains unresolved, because angular acceleration and velocity are typically confounded. Here, we developed a rhesus macaque model of postural control that independently manipulates angular acceleration and peak velocity during transient pitch and roll tilts in monkeys of either sex. By simultaneously measuring head kinematics—directly relevant to vestibular signaling—and center-of-pressure dynamics, we quantified how sensory inputs and motor outputs evolve across successive phases of the postural response. We show that short-latency postural responses (<100 ms) are primarily governed by angular acceleration, whereas medium-latency responses (100–200 ms) scale with angular velocity. This dissociation was robust across perturbation axes and accompanied by axis-dependent control strategies: roll tilts elicited constrained head motion consistent with active stabilization in space, whereas pitch tilts produced more compliant, platform-following behavior. Together, these findings identify distinct kinematic variables governing successive phases of balance control and establish a primate framework for linking neural circuit activity to the temporal organization of postural responses. Significance Statement Maintaining balance requires transforming sensory signals about unexpected body motion into precisely timed motor commands. Progress in understanding this process has been limited because angular acceleration and velocity are inherently coupled during rotational perturbations. Here, using a rhesus macaque model, we dissociate these kinematic variables and show that they govern distinct temporal phases of postural control: angular acceleration determines short-latency (<100 ms) responses, whereas angular velocity shapes medium-latency (100–200 ms) adjustments. We further demonstrate axis-dependent postural strategies that parallel those observed in humans. Together, these findings resolve a longstanding confound in balance research and establish a primate framework that will enable future studies to link neural circuit activity to the biomechanics of postural control.

  PublisherOA PDFDOI

• Eye-head coordination during goal-directed orienting in mice

  Communications Biology · 2026-04-03

  articleOpen accessSenior author

  In afoveate species such as mice, it is accepted that gaze is typically redirected by head movements with a saccade-and-fixate strategy, while the eyes primarily stabilize vision within a limited oculomotor range. This view suggests that the accompanying eye movements are primarily reflexive, driven by mechanisms like the vestibulo-ocular reflex (VOR). However, emerging evidence challenges this assumption, suggesting that eye movements during active head motion may not be purely reflex-driven. Here, we directly test whether eye movements in mice are actively coordinated as part of voluntary gaze redirection rather than being reflexive. By systematically monitoring head and pupil positions during goal-directed orienting in a cohort of male mice, we find that mice generated active saccadic eye movements whose onsets are tightly linked to head movements. Furthermore, these saccadic eye movements occur at markedly shorter latencies than reflexive quick-phase eye movements evoked by comparable passive head rotations. Importantly, the interplay between coordinated eye and head movements during voluntary orienting resemble the predictable, stereotyped gaze patterns seen in foveate animals, such as primates. Our results suggest that mice possess an evolutionarily conserved mechanism for gaze redirection, integrating voluntary eye-head coordination similar to that of foveate vertebrates. These findings reframe the prevailing view by demonstrating an actively coordinated eye-head component to gaze redirection under goal-directed conditions in mice, complementing established reflexive mechanisms.

  PublisherDOI

Recent grants

• The Physiology of Vestibular Compensation

  NIH · $11.4M · 1995–2029

• NIH Grant F31MH009843

  NIH · $12k

• Neural Computations Underlying Cancellation of the Vestibular Consequences of Voluntary Movement

  NIH · $4.0M · 2019–2029

• Mechanism and Functional Significance of Polarity Reversal in Mechanosensory Organs

  NIH · $3.5M · 2019–2025

• Trainging Program in Hearing and Balance

  NIH · $9.7M · 1985–2026

Frequent coauthors

• Kantapon Pum Wiboonsaksakul

  Discovery Institute

  100 shared

• Dale Roberts

  Johns Hopkins University

  59 shared

• Michael Strupp

  LMU Klinikum

  58 shared

• A. John Van Opstal

  Radboud University Nijmegen

  56 shared

• Jorge Otero- Millan

  Johns Hopkins Medicine

  56 shared

• Jesse Heckman

  Johns Hopkins Medicine

  56 shared

• Jacob M. Pogson

  56 shared

• Sage O. Sherman

  University of Colorado Boulder

  56 shared

Labs

• Cullen LabPI