GH-axis disruption after TBI in male juvenile rats

DOI:10.34945/F5R30F

DATASET CITATION

Rowe R. K., Ortiz J., Murphy S. M. (2023) GH-axis disruption after TBI in male juvenile rats. Open Data Commons for Traumatic Brain Injury. ODC-TBI:823 http://doi.org/10.34945/F5R30F

ABSTRACT

STUDY PURPOSE: We have previously shown that specific to the pediatric population, children with a traumatic brain injury (TBI) diagnosis have 3.22 times the risk of a subsequent endocrine diagnosis compared with the general pediatric population, with the predominant endocrine disorder diagnoses of “precocious sexual development and puberty”, followed by, “pituitary dwarfism/growth hormone deficiencies”. We used these clinical observations to inform our translational research investigating growth hormone-axis disruption following diffuse TBI in the juvenile rat. In the current study, we used post-natal day 17 rats, which model early childhood in humans, and assessed body weights, plasma growth hormone levels, and mean number of somatostatin neurons at acute and chronic time points post-injury. We hypothesized that diffuse TBI in juvenile rats would alter circulating growth hormone levels due to damage to the hypothalamus, specifically somatostatin neurons.

DATA COLLECTED: Juvenile (post-natal day 17) male rats were subjected to midline fluid percussion injury or a control sham surgery. Following the injury, we measured the righting reflex time (time it took a rat to right itself). Body weights were collected prior to surgery/injury, post-operatively at 1, 2, and 3 days post-injury, then weekly until tissue was collected at pre-determined time points post-injury (1, 7, 18, 25, 43 days post-injury). At the terminal time point blood and brains were collected. Blood was centrifuged and plasma was isolated. Growth hormone levels were measured in plasma by ELISA. Brains were cryosectioned and stained to visualize somatostatin neurons in the hypothalamus. Three investigators blinded to the experimental conditions counted all stained neurons in 6-9 images per rat. Cell counts were tabulated using ImageJ software to manually label each cell using the ROI manager. These counts were averaged across sections per rat and across investigators to determine the mean number of somatostatin neurons per image per rat.

CONCLUSIONS: Diffuse traumatic brain injury suppressed acute neurological reflexes measured as a higher righting reflex time. Brain-injured rats had a lower terminal body weight at 18 days post-injury compared to shams. Growth hormone levels increased over time but were not significantly altered by brain injury. Brain-injured rats had fewer somatostatin neurons at 1 day post-injury compared to shams. The mean number of somatostatin neurons positively predicted the growth hormone levels independent of brain injury.

KEYWORDS

concussion; Growth hormone deficiency; growth hormone; Somatostatin; puberty; development; Pediatric

PROVENANCE / ORIGINATING PUBLICATIONS

RELEVANT LINKS

NOTES

DATASET INFO

Contact: Rowe Rachel (rachel.rowe@colorado.edu)

Lab: Rachel Rowe

ODC-TBI Accession:823

Records in Dataset: 451

Fields per Record: 11

Last updated: 2023-12-01

Date published: 2023-12-01

Downloads: 4

Files: 2

LICENSE

Creative Commons Attribution License (CC-BY 4.0)

FUNDING AND ACKNOWLEDGEMENTS

National Institutes of Health R21NS120022 (RKR), Brain Injury Association of America Seed Grant (JBO, RKR)

CONTRIBUTORS

Rowe, Rachel K.

University of Colorado Boulder

Ortiz, J. Bryce

University of Arizona College of Medicine Phoenix

Murphy, Sean M.

University of Arizona College of Medicine Phoenix

Tellez, Sebastian

Arizona State University

Rampal, Giri

University of Bath

Couillard, Nicole

University of Colorado Boulder

Mendez, Matias

University of Colorado Boulder

Green, Tabitha R.F.

University of Colorado Boulder