About

Victoria Abraira is an Assistant Professor in the Department of Cell Biology and Neuroscience at Rutgers University, School of Arts and Sciences, Division of Life Sciences. She is the Director of the Cell and Developmental Biology Program and is involved in graduate programs in Cell & Developmental Biology and Microbiology & Molecular Genetics. Her major research interests include aging, behavior, developmental biology, neurological disease, and neuroscience. Her research techniques encompass bioinformatics, cell biology, fluorescent and super-resolution microscopy, genetic engineering, and imaging, primarily using humans and mice as model organisms. Her lab utilizes mouse molecular genetics to understand the sense of touch, exploring how tactile stimuli are recognized and interpreted to perceive the physical world. Her previous work as a postdoctoral fellow at Harvard Medical School focused on understanding the cellular and synaptic substrates underlying innocuous touch perception, including the functional organization of sensory neurons in mouse hairy skin and neural coding in the spinal cord dorsal horn. Currently, her research extends to dissecting touch circuits from the skin to the brain with new mouse genetic tools, aiming to develop an integrative model of touch perception in health and disease. She is recognized for her contributions to understanding somatosensation, pain, movement, spinal cord injury, systems neuroscience, and circuit neuroscience.

Research topics

• Psychology
• Neuroscience
• Medicine
• Biology
• Social psychology
• Physical medicine and rehabilitation
• Anesthesia
• Endocrinology

Selected publications

• BPS2026 – Context is the key: How spinal cord neuromodulation shapes our somatosensory experiences

  Biophysical Journal · 2026-02-01

  article1st authorCorresponding
  PublisherDOI

• Oxytocin Modulation of Spinal Circuits Drives Therapeutic Benefits of Massage

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-12 · 1 citations

  articleOpen accessSenior authorCorresponding

  Across social species, social touch enhances well-being and reduces pain - two seemingly distinct benefits that enhance survival. Yet where and how the nervous system integrates these functions, and whether a single mechanism could serve both, remains unknown. Here we show that massage triggers oxytocin release, which shapes both pain and touch reward at the earliest stage of central processing - the spinal cord - through a single, state-dependent circuit mechanism. We report that in humans, massage enhances well-being, effects that correlate with endogenous oxytocin release. In mice, gentle touch activates hypothalamic oxytocin neurons that project directly to the spinal dorsal horn. Genetic manipulation of spinal oxytocin circuits alters behavioral responses to both gentle touch and noxious stimuli. Spinal calcium imaging and slice electrophysiology reveal that oxytocin acts on both excitatory and inhibitory spinal neurons to sculpt the relative activity of spinal ascending systems that convey both social touch and pain to the brain. Extending these findings to humans, we show that oxytocin receptors are also expressed on spinal excitatory and inhibitory neurons, and that endogenous oxytocin during massage correlates with altered spinal touch processing. Thus, spinal oxytocin signaling provides an evolutionarily conserved mechanism for the therapeutic benefits of massage.

  PublisherDOI

• The composition of motor recovery revealed by syllable-level behavioral analysis after spinal cord injury

  Research Square · 2026-02-05

  preprintOpen access1st authorCorresponding
  PublisherDOI

• Functional synaptic connectivity of engrafted spinal cord neurons with locomotor circuitry in the injured spinal cord

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-04-05 · 3 citations

  preprintOpen access

  Spinal cord injury (SCI) results in significant neurological deficits, with no currently available curative therapies. Neural progenitor cell (NPC) transplantation has emerged as a promising approach for neural repair, as graft-derived neurons (GDNs) can integrate into the host spinal cord and support axon regeneration. However, the mechanisms underlying functional recovery remain poorly understood. In this study, we investigate the synaptic integration of NPC-derived neurons into locomotor circuits, the projection patterns of distinct neuronal subtypes, and their potential to modulate motor circuit activity. Using transsynaptic tracing in a mouse thoracic contusion SCI model, we found that NPC-derived neurons form synaptic connections with host locomotor circuits, albeit at low frequencies. Furthermore, we mapped the axon projections of V0C and V2a interneurons, revealing distinct termination patterns within host spinal cord laminae. To assess functional integration, we employed chemogenetic activation of GDNs, which induced muscle activity in a subset of transplanted animals. However, NPC transplantation alone did not significantly improve locomotor recovery, highlighting a key challenge in the field. Our findings suggest that while GDNs can integrate into host circuits and modulate motor activity, synaptic connectivity remains a limiting factor in functional recovery. Future studies should focus on enhancing graft-host connectivity and optimizing transplantation strategies to maximize therapeutic benefits for SCI.

  PublisherOA PDFDOI

• Categorizing treatment mechanisms for Complementary and Integrative Musculoskeletal Interventions

  International journal of osteopathic medicine · 2025-01-07 · 4 citations

  articleOpen access
  PublisherOA PDFDOI

• Functional synaptic connectivity of engrafted spinal cord neurons with hindlimb motor circuitry in the injured spinal cord

  Nature Communications · 2025-11-24 · 1 citations

  articleOpen access

  Spinal cord injury (SCI) results in significant neurological deficits, and curative therapies are lacking. Neural progenitor cell (NPC) transplantation shows promise, as graft-derived neurons (GDNs) can integrate into host spinal cord and support axon regeneration. Here, we examined the synaptic integration of GDNs into hindlimb motor circuits in a mouse thoracic contusion SCI model. Transsynaptic tracing revealed that GDNs form synaptic connections with host motor circuits. Axon mapping showed distinct termination patterns of cholinergic and V2a interneurons within host spinal cord. Chemogenetic activation of GDNs induced muscle activity in a subset of transplanted animals, but NPC transplantation alone did not improve locomotor recovery. These findings indicate that GDNs can integrate into and modulate activity of host circuits, yet limited synaptic connectivity constrains functional recovery. Future studies should enhance graft-host connectivity and refine transplantation strategies to maximize therapeutic benefit for SCI. Neural progenitor cell transplantation shows promise for treating spinal cord injury. However, here, the authors show that graft-derived neurons form limited synaptic connections with host spinal motor circuits after injury, constraining functional motor recovery.

  PublisherOA PDFDOI

• The dorsal column nuclei scale mechanical sensitivity in naive and neuropathic pain states

  Cell Reports · 2025-04-01 · 5 citations

  articleOpen accessSenior author

  During pathological conditions, tactile stimuli can aberrantly engage nociceptive pathways leading to the perception of touch as pain, known as mechanical allodynia. The brain stem dorsal column nuclei integrate tactile inputs, yet their role in mediating tactile sensitivity and allodynia remains understudied. We found that gracile nucleus (Gr) inhibitory interneurons and thalamus-projecting neurons are differentially innervated by primary afferents and spinal inputs. Functional manipulations of these distinct Gr neuronal populations bidirectionally shifted tactile sensitivity but did not affect noxious mechanical or thermal sensitivity. During neuropathic pain, Gr neurons exhibited increased sensory-evoked activity and asynchronous excitatory drive from primary afferents. Silencing Gr projection neurons or activating Gr inhibitory neurons in neuropathic mice reduced tactile hypersensitivity, and enhancing inhibition ameliorated paw-withdrawal signatures of neuropathic pain and induced conditioned place preference. These results suggest that Gr activity contributes to tactile sensitivity and affective, pain-associated phenotypes of mechanical allodynia.

  PublisherDOI

• Remote automated delivery of mechanical stimuli coupled to brain recordings in behaving mice

  eLife · 2025-09-08

  articleOpen access

  Summary The canonical framework for testing pain and mechanical sensitivity in rodents is manual delivery of stimuli to the paw. However, this approach is time consuming, produces variability in results, requires significant training, and is ergonomically unfavorable to the experimenter. To circumvent limitations in manual delivery of stimuli, we have created a device called the ARM (Automated Reproducible Mechano-stimulator). Built using a series of linear stages, cameras, and stimulus holders, the ARM is more accurate at hitting the desired target, delivers stimuli faster, and decreases variability in delivery of von Frey hair filaments. We demonstrate that the ARM can be combined with traditional measurements of pain behavior and automated machine-learning based pipelines. Importantly, the ARM enables remote testing of mice with experimenters outside the testing room. Using remote testing, we found that mice habituated more quickly when an experimenter was not present and experimenter presence leads to significant sex-dependent differences in paw withdrawal and pain associated behaviors. Lastly, to demonstrate the utility of the ARM for neural circuit dissection of pain mechanisms, we combined the ARM with cellular-resolved microendoscopy in the amygdala, linking stimulus, behavior, and brain activity of amygdala neurons that encode negative pain states. Taken together, the ARM improves speed, accuracy, and robustness of mechanical pain assays and can be combined with automated pain detection systems and brain recordings to map central control of pain.

  PublisherDOI

• MASSAG model: Towards an integrative neuroscience framework linking emotional trauma, pain, and mechanisms of force-based manipulations

  Neuroscience & Biobehavioral Reviews · 2025-12-09 · 1 citations

  reviewOpen access

  The frequent comorbidity of chronic pain, affective disorders, and trauma histories suggests shared mechanisms, and opportunities for interventions that target their overlap. Force-based manipulations (FBMs) of the soft tissues such as massage and fascial manipulation are especially relevant given their dual impact on sensory and affective mechanisms. This paper synthesizes current evidence on the distributed somatosensory effects of emotional trauma, evaluating how trauma and stress reshape neural, immune, and connective tissue functions, altering sensory perception and pain processing. By elucidating known as well as plausible mechanisms, we aim to provide a foundation for advancing research on how FBMs of the soft tissues may counter stress and trauma-related alterations in the somatosensory system. We then propose the MASSAG (Mechanisms of Affective Somatosensory Soothing for Allostatic Gain) model, which is intended to provide a framework for understanding the therapeutic benefit of manual therapies and to guide future research in this field. This integrative framework conceptualizes how manipulation of the soft tissues engage both sensory-afferent and cognitive-affective pathways ideally situated to reshape predictive models of somatosensory experience and counter the long-term effects of trauma and pain.

  PublisherDOI

• Author response: Remote automated delivery of mechanical stimuli coupled to brain recordings in behaving mice

  2025-10-17

  peer-reviewOpen access
  PublisherDOI

Recent grants

• NIH Grant F31DC008450

  NIH · $86k · 2009

• Anatomical, physiological, and behavioral correlates of a C-LTMR circuit

  NIH · $161k · 2011–2014

Frequent coauthors

• David D. Ginty

  Harvard University

  31 shared

• Manon Bohic

  Rutgers, The State University of New Jersey

  27 shared

• Emily D. Kuehn

  Harvard University

  25 shared

• Ishmail Abdus-Saboor

  Columbia University

  20 shared

• William Foster

  Howard Hughes Medical Institute

  17 shared

• Mark A. Gradwell

  Rutgers, The State University of New Jersey

  17 shared

• Ling Bai

  Nanjing University of Chinese Medicine

  17 shared

• Aman Upadhyay

  Rutgers, The State University of New Jersey

  14 shared

Awards & honors

• Rita Allen Foundation Scholar