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Laboratory of Coleen M. Atkins, Ph.D.

Dr. Coleen Atkins and Lab Members
Dr. Coleen Atkins and Lab Members

Our Current Lab Projects


  • Therapies to Reduce Inflammation After Traumatic Brain Injury
  • Circuitry Remodeling in the Chronic Injured Brain
  • Concussions Sustained When Exercising in Warm Temperatures



Atkins - Therapies to reduce inflammation after TBFlow figure
Atkins – Therapies to reduce inflammation after TBFlow figure

Every year an estimated 1.7 million people suffer a traumatic brain injury (TBI). The initial brain trauma triggers a complex inflammatory response; this acute inflammatory response increases neuronal death and worsens outcome after TBI. The inflammatory response is regulated by a diverse array of molecules; one of these molecules is the highly ubiquitous second messenger, cAMP. Inhibition of a cAMP-hydrolyzing enzyme, phosphodiesterase 4 (PDE4), has been used as an anti-inflammatory strategy in models of systemic inflammation and CNS injury. We have found that the PDE4B isoform, PDE4B2, is elevated acutely after TBI; additionally, we found that PDE4B2 is upregulated in microglia and infiltrating leukocytes at 24 hours after TBI. Currently, we are exploring the anti-inflammatory potential of cAMP elevation after TBI using isoform-selective inhibitors of PDE4.


Circuitry remodeling in the chronic injured brain
Circuitry remodeling in the chronic injured brain

Profound neuronal circuit changes occur within the hippocampus that chronically hinder recovery of cognitive functioning after traumatic brain injury (TBI). Principal changes during the chronic recovery phase of brain injury include a depression in basal synaptic transmission and impaired expression of long-term potentiation in area CA1 of the hippocampus. Multiple studies report that normal hippocampal electroencephalograph oscillatory patterns in the 6-10 Hz range are reduced after TBI. These theta rhythms are responsible for arousal, sensorimotor processing and promote LTP expression in the hippocampus to encode spatial memory. The hippocampal theta rhythm arises from cholinergic projections from the medial septum via the fimbria-fornix. Atrophy in the fimbria-fornix is routinely observed in TBI survivors and suggests that the cholinergic tone required for establishing theta rhythm is deficient. These changes are reminiscent of Alzheimer’s disease and age-related mild cognitive impairment where targeting the cholinergic system restores hippocampal theta rhythm and promotes learning and memory in the dysfunctional brain. We are currently testing strategies to restore theta rhythm after TBI and rescue chronic learning and memory deficits. By targeting both the cholinergic system and the GABAergic system, we can improve basal synaptic transmission, rescue long-term potentiation and chronic learning and memory deficits after TBI.


Concussions Sustained when Exercising in Warm Temperatures
Concussions Sustained when Exercising in Warm Temperatures

Many athletes and soldiers are susceptible to mild traumatic brain injury (TBI) while experiencing high temperature environments. Mild traumatic brain injury (TBI) typically does not elicit gross pathological changes to the brain. However, many athletes and soldiers experience mild TBI in the context of mild hyperthermia (39ºC). This mild elevation in brain temperature can convert the minimal pathology caused by a mild TBI into a pathology resembling a moderate TBI. We have recently discovered that this results in significant learning and memory deficits that persist for weeks after the mild brain injury. The elevation of brain and body temperature from strenuous physical exercise can be easily reduced by cessation of the activity and cooling strategies such as ice packs and ingestion of cold liquids. Therefore, we are testing the optimal cooling strategies to reduce neurological problems from concussion sustained when exercising in warm temperatures.

Name Phone Email
Dr. David Titus 305-243-4926
Dr. Fabiola Placeres 305-243-7113
Nathan Johnson 305-243-4926