Department of Neurobiology
Room 4.212D Research Building 17
Route: 0620 | Tel: (409) 747-2214 | bochen1@utmb.edu

Education and Training
B.Sc. Biological science, University of Birmingham, Birmingham, U.K.
M.Sc. Biomedical science, Durham University, Durham, U.K.
Ph.D. Applied biomedical science, University of Reading, Reading, U.K.
Postdoctoral training, Boston Children’s Hospital, Harvard Medical School, Boston, U.S.

Research Overview
Our ultimate goal is to develop translational therapies that improve quality of life for people with spinal cord injury (SCI) and other central nervous system (CNS) disorders and trauma.  We focus on what matters most to patients—motor recovery, bladder and bowel control, pain relief, and sexual function. By studying how SCI changes spinal neurons, circuits, and physiology, we design treatments that prevent harmful remodeling and strengthen communication between the brain and spinal cord.

KCC2 agonist may unlock spared pathways to restore stepping after incomplete SCI
Most SCIs are anatomically incomplete, leaving axons that still cross the injury. We aim to harness these spared pathways to drive recovery. Using a targeted experimental model, we found that spinal inhibitory interneurons can block descending signals from engaging relay circuits after injury. Enhancing KCC2—a chloride transporter that reduces neuronal over-inhibition—with selective agonists releases this brake and improves stepping in our models. Open questions remain:  how does KCC2 change across specific neuron types, and what are the precise consequences of its pathological dysregulation? Using multiple injury models and new tools, we are dissecting cell-specific KCC2 mechanisms and testing strategies to prevent these pathological changes at their source.


Preventing pathological neuron changes to improve motor function
SCI causes swelling of spinal neurons, but its role in neuron loss and functional deficits has been unclear. In our mouse models, we find that both excitatory and inhibitory neurons swell and degenerate, each with distinct timelines. To map these changes, we developed a 3D image-analysis pipeline that quantifies neuron types, numbers, volumes, and spatial distribution. Using these tools, we’re testing mechanisms and interventions that prevent neuronal swelling and cell loss to support better motor recovery. 

Reconnecting PMC-spinal pathways to bring back voluntary bladder control
Voluntary bladder control depends on descending signals from the brain that coordinate the pontine micturition center (PMC) with lumbosacral spinal circuits—timing bladder contraction with sphincter relaxation. SCI disrupts these pathways, causing loss of control and other bladder dysfunctions. We map PMC–spinal relay circuits in intact and injured spinal cords and test ways to re-engage them. Our goal is to build a mechanistic foundation for neural repair—such as circuit-specific stimulation or pharmacologic modulation—to restore bladder function after SCI.

Targeting maladaptive brain-to-spinal pathways to stop CNP at its source
Central neuropathic pain (CNP) affects roughly half of people with SCI and can severely diminish quality of life. Using a T8 lateral hemisection model—the rodent analogue of Brown-Séquard syndrome that reproduces key CNP features—we investigate how maladaptive descending pathways, and spinal circuits drive persistent pain. With this clinically relevant model, we are mapping cellular and circuit mechanisms, identifying points of intervention, and test strategies to prevent CNP development and reduce established pain.

Selected Publications:

2020-2025 @ UTMB (*indicates UTMB-led research project)

*Henwood, M., et al., Yuan, S., & Chen, B. (2025). Sensory deficits in mice with lateral spinal cord hemisection mimic the Brown-Séquard syndrome. Journal of Neuroscience (In press).

Metwally, S., et al., & Sun, D. (2025). Cerebellum KCC2 protein expression plasticity in response to cerebral cortical stroke. Neurochemistry International, 184, 105939.

Huang, S., et al., & Rao, S. (2025). Anisotropic hydrogel microelectrodes for intraspinal neural recordings in vivo. Nature Communications, 16, 1127.

*Sandoval, A., & Chen, B. (2024). Regenerative and repair strategies for the central nervous system: Progress in basic and clinical research on spinal cord injury. In Neuroimmune Pharmacology and Therapeutics (pp. 975–985). Springer Nature Switzerland.

*Li, Q., et al., & Chen, B. (2024). Reduction of prolonged excitatory neuron swelling after spinal cord injury improves locomotor recovery in mice. Science Translational Medicine, 16, eadn7095.

*Li, Q., et al., & Chen, B. (2023). Advancing spinal cord injury research with optical clearing, light sheet microscopy, and artificial intelligence-based image analysis. Neural Regeneration Research, 18(12), 2661–2662.

*Yu, H., et al., & Chen, B. (2022). Pipeline for fluorescent imaging and volumetric analysis of neurons in cleared mouse spinal cords. STAR Protocols, 3, 101759.

*Brommer, B., et al., Chen, B., & He, Z. (2021). Improving hindlimb locomotor function by non-invasive AAV-mediated manipulations of propriospinal neurons in mice with complete spinal cord injury. Nature Communications, 12, 498.

Li, Y., et al., & He, Z. (2020). Microglia-organized scar-free spinal cord repair in neonatal mice. Nature, 587, 613–618.

Pre-2020

Chen, B., Li, Y., et al., & He, Z. (2018). Reactivation of dormant relay pathways in injured spinal cord by KCC2 manipulations. Cell, 174, 521–535.e13.

Liu, Y., Latremoliere, A., et al., & He, Z. (2018). Touch and tactile neuropathic pain sensitivity are set by corticospinal projections. Nature, 561, 547–550.

Liu, Y., Wang, X., et al., & He, Z. (2017). A sensitized IGF1 treatment restores corticospinal axon-dependent functions. Neuron, 95, 817–833.e4.