Yadiel Alicea-Torres^1,2, Eduardo Rosario-Díaz^1,2, Paulette Vázquez-Martínez^1,2, Gabriela Serrano-Rivera^1,2, Diego Nazario-Martínez^1,2, Joseph Torres-Cruz^1,2, Isabel Rivera-Correa^1,2, Jahaziel Díaz-Rodríguez^1,2, Génesis Rivas-Soto, Laura Vicente-Rodríguez, PhD^1,2, Demetrio Sierra-Mercado, PhD²

¹University of Puerto Rico at Cayey, Department of Biology, ²University of Puerto Rico, Medical Sciences Campus, Department of Anatomy and Neurobiology

Introduction: Concussive brain injury is more prevalent in females than in males. Moreover, females are more likely to display increased anxiety after a concussion. Rodent models can be useful to simulate concussion and study their behavioral sequelae. We hypothesized that concussive brain injury would increase anxiety-like behaviors in females.

Methods: To test this idea, we used a closed head injury model via weight-drop to mimic concussive injury in adult, female rats. We then studied anxiety-like behaviors using the open field test (OFT) at varying time points after injury. Specifically, rats (CHI: n=12, SHAM: n=12) were exposed to the OFT on days 4, 8, 13 and 17 post injury for 10-minute recording sessions. In each session, we recorded the distance travelled, and time spent in the center of the open field, which is the part of the open field thought to be most anxiogenic.

Results: Our results demonstrate that rats delivered CHI displayed increased distance travelled compared to SHAM controls (p=0.0029), and increased time spent in the center of the open field (p<0.001). Contrary to our initial hypothesis, the results of the OFT suggest that CHI decreases anxiety. Indeed, decreased levels of anxiety could be problematic since normal levels of anxiety are necessary for survival.

Conclusion: Next, to gain insight on how CHI affected the brain, we will use immunohistochemistry to evaluate neuronal activity in brain regions involved in anxiety-like behaviors, such as the insular cortex and subregions of the prefrontal cortex. Results from this study will serve as a foundation for further understanding neuronal mechanisms involved in detrimental effects post injury.

IACUC approval number: A 120121

Acknowledgments: NIEHS R21ES034191 to DS-M and FG-V; NINDS R21NS119991, Brain & Behavior Research Foundation Young Investigator grant, PRCTRC Pilot, NIGMS COBRE II, RCMI8G12MD00760, Hispanics in Research Capability (HiREC), and Title V Pilot Project (PiP)  to DS-M; NSF PRCEN fellowships to MC-C, MR-L& HH-M, Neuro-ID fellowship 5R25NS080687 to TS-R, AF-P & GH-B, UPR Med Sci Campus Chancellor’s Office and School of Medicine Deanship.