A photo of Steven Crone.

Assistant Professor, UC Department of Pediatrics


Biography & Affiliation


The nervous system is a complex network of nerves that sends messages between the brain and spinal cord to all areas of the body. Without a healthy nervous system, humans would be unable to walk, write, hug, breathe or speak.

My research areas are in neuroscience and physiology. In our lab, we study neuroscience and physiology to better understand the nervous system and how it upholds ventilation and suitable blood gasses to support life.

The research goals of my team include 1) understanding what occurs with neural circuits that control breathing in patients with disease or after injury, and 2) how we could enhance the function of those circuits to strengthen breathing and the quality of patients’ lives.

My research interests stem from my training in the development and function of brainstem and spinal cord circuits used in breathing and movement. I decided to focus on breathing because ventilator dependence greatly affects these patients' quality of life, and respiratory failure is one of the most common causes of death in neurodegenerative diseases and following spinal cord injury.

In my lab at the Cincinnati Children's Hospital Medical Center, we study what happens to breathing circuits after disease (amyotrophic lateral sclerosis, spinal muscular atrophy, epilepsy) and spinal cord injury. We want to translate our research discoveries into possible treatments for patients. One of the most significant discoveries that my team and I made is identifying neurons in the spinal cord that are imperative for controlling accessory respiratory muscles. These muscles are necessary for humans to breathe when exercising or when people need more ventilation. Furthermore, these muscles are necessary for compensating during impaired diaphragm function due to neuromuscular disease or injury.

We also found that neurons important for controlling accessory respiratory muscles degenerate in the spinal cord and brainstem in an amyotrophic lateral sclerosis (ALS) mouse model. Accessory respiratory muscles become active in patients with ALS to help them compensate for feeble muscle strength when attempting to breathe. However, at late stages of the disease, these patients exhibit a severe decrease in breathing when they can no longer compensate for diaphragm weakness. Our studies indicate that preventing degeneration of spinal neurons or improving the function of spared circuitry could help patients breathe better and postpone the need for mechanical ventilation.

Another research goal is to find medicines that could target spinal circuits and restore breathing to patients with a cervical spinal cord injury. Many of these patients cannot breathe without a ventilator. We found that raising the excitability of a certain population of spinal cord neurons can restore function to a formerly paralyzed diaphragm in a mouse model of spinal cord injury.

Recognitions I’ve received include an Emerging Investigator Award (2013) from the Gwendolyn Strong Foundation and FightSMA.

I first started working at the Cincinnati Children’s Hospital Medical Center in 2012 and have more than twenty-five years of experience in the neuroscience field. I’ve also published papers in multiple journals, including Frontiers in Systems Neuroscience, Experimental Neurology and Cell Reports.

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Research Divisions

Developmental Biology, Neurosurgery, Neuromuscular Development


BS: The Pennsylvania State University, University Park, PA, 1995.

PhD: University of California, San Diego and The Salk Institute for Biological Studies, San Diego, CA, 2003.

Postdoctoral: University of Chicago, Chicago, IL, 2012.


Role of Propriospinal Neurons in Control of Respiratory Muscles and Recovery of Breathing Following Injury. Jensen, VN; Alilain, WJ; Crone, SA. Frontiers in Systems Neuroscience. 2020; 13.

V2a Neurons Constrain Extradiaphragmatic Respiratory Muscle Activity at Rest. Jensen, VN; Seedle, K; Turner, SM; Lorenz, JN; Crone, SA. eNeuro. 2019; 6.

Increasing the excitability of V2a neurons restores diaphragm function following spinal cord injury. JENSEN, VN; Alilain, W; Crone, SA. FASEB Journal. 2019; 33:731.1-731.1.

Corticospinal Circuits from the Sensory and Motor Cortices Differentially Regulate Skilled Movements through Distinct Spinal Interneurons. Ueno, M; Nakamura, Y; Li, J; Gu, Z; Niehaus, J; Maezawa, M; Crone, SA; Goulding, M; Baccei, ML; Yoshida, Y. Cell Reports. 2018; 23:1286-1300.e7.

Increasing or decreasing the excitability of V2a neurons activates accessory respiratory muscles. Jensen, VN; Seedle, K; Turner, SM; Crone, SA. FASEB Journal. 2018; 32:893.2-893.2.

Repeated Measurement of Respiratory Muscle Activity and Ventilation in Mouse Models of Neuromuscular Disease. Jensen, VN; Romer, SH; Turner, SM; Crone, SA. Journal of Visualized Experiments. 2017.

Accessory respiratory muscles enhance ventilation in ALS model mice and are activated by excitatory V2a neurons. Romer, SH; Seedle, K; Turner, SM; Li, J; Baccei, ML; Crone, SA. Neurodegeneration : a journal for neurodegenerative disorders, neuroprotection, and neuroregeneration. 2017; 287:192-204.