Traumatic Brain Injury Group

football helmet and brain in a jar on a shelf

Mild traumatic brain injury (TBI), also known as concussion, is an important public health issue because of its prevalence and potentially serious and lasting effects on mood, memory, and sensory and motor function, all of which adversely affect well-being. Some of the effects on mood, such as depression, anxiety and irritability, overlap those of post-traumatic stress disorder (PTSD), an issue facing many military personnel, and as a result PTSD is often regarded as one outcome of TBI. The spinal cord can be injured by the same concussive forces that damage the brain, such as in an automobile collision, and result in motor impairment. Moreover, those experiencing multiple concussions are at increased risk for such debilitating neurodegenerative diseases as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). Multiple concussions or even repeated subconcussive blows to the head can also lead to the progressive degenerative disease that was originally called pugilistica dementia when it was thought to be limited largely to boxers. This disease is characterized by memory loss, depression, irritability and a specific type of brain pathology, and is now referred to as chronic traumatic encephalopathy (CTE), since it has been seen in some individuals engaged in high-impact sports (football, soccer, hockey, rugby) and in professions where repeated head impact is common, such as the military.

Researchers and clinicians at UTHSC are investigating how traumatic injury to the nervous system produces adverse consequences for mood, memory, and sensory and motor function, and are seeking to develop appropriate treatments.  To this end, Anton Reiner and Marcia Honig of the Department of Anatomy & Neurobiology have developed mouse models of concussive injury to the brain and spinal cord to examine the role of axonal injury, neuron loss, and neuroinflammation in the neuropsychiatric, visual and motor deficits after such injuries.  The role of specific patterns of neuronal loss in the amygdala, a structure long known to be involved in emotion, in the PTSD-like symptoms after TBI is being studied with Scott Heldt (Department of Anatomy & Neurobiology), and the role of electrophysiological abnormalities in frontal cortex (which are also involved in emotion and executive function) in the PTSD-like symptoms are being studied with Detlef Heck (Department of Anatomy & Neurobiology).  

axonal bulbs in mouse spinal cord

The axons shown were genetically engineered to produce a yellow fluorescent protein so they can be visualized.  These particular axons arise in the brain, and in the image are coursing from left to right as they descend the spinal cord.  The axonal damage is evidenced by the many prominent thickenings called bulbs, which form when axons are stretched and microtubules within them break.  Cellular components that are normally transported down the axon along microtubules accumulate above those break points, causing the axon to swell. 


This research group is also testing therapies that improve the recovery from sensory, motor and neuropsychiatric deficits after mild TBI. For example, together with Bob Moore of the Department of Pharmaceutical Sciences, drug therapies that control the neuroinflammatory response to neural injury and thereby improve the recovery after mild TBI are being tested. The value of adipose-derived stem cells as a treatment for the ocular injury after concussion is being assessed with Shekhar Gangaraju (Department of Ophthalmology), and the benefits of prolonged sedation in the recovery from concussion are being evaluated with Edward Chaum (Department of Ophthalmology).

Doctors Reiner, Heck, and Moore

A $418,000 grant from the National Institute of Neurological Disorders and Strokes will allow Dr. Hetlef (center, pictured with Dr. Anton Reiner (left) and Dr. Bob Moore, to explore treatment options for mild traumatic brain injury.




 Microglia in optic tract control and concussed

The images show that concussion causes activation of cells in the brain called microglia, which then react producing ‘neuroinflammation’ that intensifies the damage. The first image shows normal microglia in the optic tract of a mouse, labeled for a protein called ionized calcium-binding adapter molecule 1 (IBA1), three days after a control procedure in which no concussion occurred. Normal microglia have small cell bodies and several thin processes. Three days after concussive injury, many microglia in the optic tract are activated – they are intensely rich in IBA1, have enlarged cell bodies, and fewer, shorter and thicker processes. After repetitive concussion (4 concussions spaced a week apart) microglial activation is even more pronounced, and persists for at least 4 months. A drug therapy we are currently studying is designed to quell microglial activation and neuroinflammation, and reduces the damage and functional deficits that concussion would otherwise produce.


Drs. Reiner and Honig, together with Mike Levin of the Department of Neurology and the Veterans Administration Medical Center, are also studying the mechanisms responsible for the long-term neurodegenerative process initiated by single or multiple TBI that leads to Alzheimer’s disease, Parkinson’s disease, ALS and CTE. Jack Tsao, also of the Department of Neurology and the Veterans Administration Medical Center, is treating military victims of TBI and seeking to develop improved treatment options using animal models. To better understand the risks of sports concussions and identify treatment approaches to enhance recovery, Asim Choudhri (Department of Radiology), Shalini Narayana (Department of Pediatrics), and Brandon Baughman (Department of Neurosurgery) are using imaging and psychological profiling methods in human subjects, while Andy Papnicolaou (Department of Pediatrics) has used magneto-encephalography to study how concussion alters communication between different brain regions. Finally, Brad Roper and Ellen Crouse of the Department of Psychiatry and the Veterans Administration Medical Center treat veterans suffering from PTSD.

Together these workers form a collaborative team investigating how concussive trauma leads to neuronal and axonal injury in the eye, brain, and spinal cord, and thereby causes diverse visual, motor, and neuropsychiatric impairments. Those wishing to support this work can make donations to the TBI and PTSD Research Fund or to the Spinal Cord Fund, using the links provided to the right. For more information contact: Anton Reiner at

TBI from control vs concussed in basolateral amygdala

Images showing that traumatic brain injury from a concussive blow causes loss of fear-reducing neurons in the basolateral amygdala, a major fear-control center of the brain.  The images shown are from mice in which the fear-reducing neurons have been genetically engineered to produce yellow fluorescent protein.  The image to the left shows fear-reducing neurons in the normal basolateral amygdala, and on the right the image shows a reduction in these neurons following concussion.  Treatments that reduce loss of these neurons or aid their function appear to reduce the PTSD-like symptoms found after concussion.

Those wishing to support this work can make donations to the TBI and PTSD Research Fund or to the Spinal Cord Fund. For more information contact: Anton Reiner at

Team Members

Anatomy & Neurobiology

Anton Reiner 
Marcia Honig
Scott Heldt
Detlef Heck

Pharmaceutical Sciences

Bob Moore


Shekhar Gangaraju
Edward Chaum

Neurology & VAMC

Mike Levin
Jack Tsao


Asim Choudhri


Shalini Narayana
Andrew Papnicolaou


Brandon Baughman

Psychiatry & VAMC

Brad Roper
Ellen Crouse

Contact Us

Neuroscience Institute
University of Tennessee Health Science Center
875 Monroe Ave, Suite 426
Memphis, TN 38163
Phone: (901) 448-5960
Fax: (901) 448-4685

Physical Address
426 Wittenborg Anatomy Building

William E. Armstrong, PhD

Anton J. Reiner, PhD

Administrative Aide:
Mistie Brewer

Program Coordinator/

Brandy Fleming, MS

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