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Cited by 60

The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.

Diffuse traumatic brain injury affects chronic corticosterone function in the rat

Rowe, Rachel K, Rumney, Benjamin M, May, Hazel G, Permana, Paska, Adelson, P David, Harman, S Mitchell, Lifshitz, Jonathan, Thomas, Theresa C·2016·Endocrine Connections
DOI 10.1530/ec-16-0031
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Abstract

As many as 20–55% of patients with a history of traumatic brain injury (TBI) experience chronic endocrine dysfunction, leading to impaired quality of life, impaired rehabilitation efforts and lowered life expectancy. Endocrine dysfunction after TBI is thought to result from acceleration–deceleration forces to the brain within the skull, creating enduring hypothalamic and pituitary neuropathology, and subsequent hypothalamic–pituitary endocrine (HPE) dysfunction. These experiments were designed to test the hypothesis that a single diffuse TBI results in chronic dysfunction of corticosterone (CORT), a glucocorticoid released in response to stress and testosterone. We used a rodent model of diffuse TBI induced by midline fluid percussion injury (mFPI). At 2months postinjury compared with uninjured control animals, circulating levels of CORT were evaluated at rest, under restraint stress and in response to dexamethasone, a synthetic glucocorticoid commonly used to test HPE axis regulation. Testosterone was evaluated at rest. Further, we assessed changes in injury-induced neuron morphology (Golgi stain), neuropathology (silver stain) and activated astrocytes (GFAP) in the paraventricular nucleus (PVN) of the hypothalamus. Resting plasma CORT levels were decreased at 2months postinjury and there was a blunted CORT increase in response to restraint induced stress. No changes in testosterone were measured. These changes in CORT were observed concomitantly with altered complexity of neuron processes in the PVN over time, devoid of neuropathology or astrocytosis. Results provide evidence that a single moderate diffuse TBI leads to changes in CORT function, which can contribute to the persistence of symptoms related to endocrine dysfunction. Future experiments aim to evaluate additional HP-related hormones and endocrine circuit pathology following diffuse TBI.

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Metadata

Authors
Rowe, R. K., Rumney, B. M., May, H. G., Permana, P., Adelson, P. D., Harman, S. M., Lifshitz, J., & Thomas, T. C.
Affiliations
  • 1Phoenix Veterans Affairs Health Care SystemPhoenix, Arizona, USA
  • 2BARROW Neurological Institute at Phoenix Children’s HospitalPhoenix, Arizona, USA
Venue
Endocrine Connections
Publisher
Bioscientifica
Published
2016-07
Volume
5
Issue
4
Pages
152-166
ISSN
2049-3614
DOI
10.1530/ec-16-0031
Cited by
60
References
16
Licence
creativecommons.org/licenses/by-nc/4.0/ (unspecified)

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