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Repetitive Blast Exposure Drives Chronic Pain in Female Rats.

Amirah Wright¹, Susan F Murphy¹, Pamela J VandeVord^1,2

¹Department of Biomedical Engineering and Mechanics, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.

Journal of Neuroscience Research

|December 18, 2025

Summary

Repeated blast traumatic brain injury (rbTBI) in female rats caused chronic pain, anxiety, and depression. These behaviors were linked to glial activation, not neuropeptide changes, in the brain.

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Area of Science:

Neuroscience
Traumatic Brain Injury Research
Pain Medicine

Background:

Clinical studies link repeated blast traumatic brain injury (rbTBI) to chronic pain with sex-dependent differences.
Preclinical models often lack systematic investigation of female subject outcomes after rbTBI.

Purpose of the Study:

To assess chronic pain behaviors and neuropathological changes in female rats following repeated blast exposures.
To investigate the underlying mechanisms, specifically glial activation and neuropeptide expression, in female rbTBI models.

Main Methods:

Adult female rats were exposed to repeated blast events.
Behavioral tests were conducted to assess mechanical/thermal hypersensitivity, anxiety, and depression-like behaviors.
Neuropathological changes were examined via glial markers (GFAP, IBA-1) and neuropeptide markers (CGRP, SP) in brain regions.

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Main Results:

Repeated blast exposure induced persistent mechanical and thermal hypersensitivity from 48 hours to 12 weeks post-injury.
Anxiety and depressive-like behaviors were observed at the chronic time point (12 weeks).
Increased glial activity (GFAP, IBA-1) was found in the frontal cortex and posterior nucleus, while CGRP and SP levels remained unchanged.

Conclusions:

Chronic pain behaviors following rbTBI in females are primarily mediated by sustained glial activation.
Neuropeptide dysregulation does not appear to be the primary driver of these chronic pain conditions in this model.
This study highlights the importance of investigating sex-specific mechanisms in rbTBI-induced chronic pain.