Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

HSV-1 reactivation as an emergent property of neuronal stress: implications for traumatic brain injury.

Journal of neuroinflammation·2026
Same author

Bridging the outcome documentation gap in epilepsy surgery: Validating large language model agents for automated Engel and International League Against Epilepsy scoring from clinical notes.

Epilepsia·2026
Same author

The Feasibility and Acceptability of Mobilizing Community Paramedics to Provide the Standard of Care for Pediatric Concussion: Mobile Integrated Health Programing for Pediatric Patients.

Prehospital emergency care·2026
Same author

Respiratory symptoms and pulmonary physiologic outcomes among post-9/11 veterans with blast exposure.

Frontiers in public health·2026
Same author

Decompression with or without Duraplasty for Chiari I and Syringomyelia.

The New England journal of medicine·2026
Same author

Mechanisms linking sleep, innate immunity, and neuroinflammation.

Brain, behavior, and immunity·2026
Same journal

The application of artificial intelligence in adrenal imaging: current state of knowledge, challenges, and future directions.

Endocrine connections·2026
Same journal

Gene expression profiles associated with stimulus-responsive insulin secretion in insulinoma.

Endocrine connections·2026
Same journal

Post-bariatric hypoglycaemia: from altered gut physiology to targeted therapies.

Endocrine connections·2026
Same journal

Group education improves self-management of adrenal insufficiency in patients and their relative.

Endocrine connections·2026
Same journal

Dampened HPG axis activity and altered ovarian gene transcription in Dummerstorf high-fertility mouse line FL2.

Endocrine connections·2026
Same journal

Interpreting salivary cortisol thresholds in ectopic ACTH syndrome.

Endocrine connections·2026
See all related articles

Related Experiment Video

Updated: Mar 19, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

29.9K

Diffuse traumatic brain injury affects chronic corticosterone function in the rat.

Rachel K Rowe1, Benjamin M Rumney2, Hazel G May2

  • 1Phoenix Veterans Affairs Health Care SystemPhoenix, Arizona, USA BARROW Neurological Institute at Phoenix Children's HospitalPhoenix, Arizona, USA Department of Child HealthUniversity of Arizona College of Medicine - Phoenix, Phoenix, Arizona, USA.

Endocrine Connections
|June 19, 2016
PubMed
Summary
This summary is machine-generated.

A single traumatic brain injury (TBI) can cause chronic endocrine issues, specifically affecting corticosterone (CORT) regulation. This dysfunction, observed in rodent models, may persist long-term, impacting patient recovery and health.

Keywords:
TBIconcussioncorticosteronestress

More Related Videos

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

9.1K
Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

5.3K

Related Experiment Videos

Last Updated: Mar 19, 2026

Controlled Cortical Impact Model for Traumatic Brain Injury
05:30

Controlled Cortical Impact Model for Traumatic Brain Injury

Published on: August 5, 2014

29.9K
Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

9.1K
Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines
09:46

Rat Model of Widespread Cerebral Cortical Demyelination Induced by an Intracerebral Injection of Pro-Inflammatory Cytokines

Published on: September 21, 2021

5.3K

Area of Science:

  • Neuroendocrinology
  • Traumatic Brain Injury Research
  • Hormonal Regulation

Background:

  • Traumatic brain injury (TBI) affects 20-55% of patients with chronic endocrine dysfunction.
  • This dysfunction is linked to hypothalamic-pituitary neuropathology and impaired quality of life.
  • The precise chronic endocrine changes post-TBI require further investigation.

Purpose of the Study:

  • To test if a single diffuse TBI causes chronic dysfunction in corticosterone (CORT) and testosterone levels.
  • To investigate the impact of TBI on the hypothalamic-pituitary endocrine (HPE) axis regulation.

Main Methods:

  • A rodent model of diffuse TBI (midline fluid percussion injury) was utilized.
  • Circulating CORT levels were measured at rest, under stress, and after dexamethasone administration at 2 months post-injury.
  • Testosterone levels, neuron morphology, neuropathology, and astrocyte activation in the hypothalamic paraventricular nucleus (PVN) were assessed.

Main Results:

  • Resting CORT levels were decreased 2 months post-TBI.
  • A blunted CORT increase was observed in response to restraint stress.
  • Altered neuron process complexity in the PVN was noted, without significant neuropathology or astrocytosis.

Conclusions:

  • A single moderate diffuse TBI induces chronic changes in CORT regulation.
  • These CORT dysfunctions may contribute to persistent endocrine dysfunction symptoms after TBI.
  • Further research will explore other hypothalamic-pituitary hormones and endocrine circuit pathology post-TBI.