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Author Spotlight: Deciphering the Long-Term Effects of Low-Level Blast Exposures in Mice
Published on: May 24, 2024
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Analgesic Modulation of Neuroendocrine and Region-Specific Neuropathological Responses Following Blast-Induced
Rex Jeya Rajkumar Samdavid Thanapaul1, Manoj Y Govindarajulu1, Mital Y Patel1
1Blast-Induced Neurotrauma Branch, Center for Military Psychiatry and Neuroscience, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA.
Journal of Neurotrauma
|April 17, 2026
Summary
Preinjury administration of buprenorphine (BUP) or meloxicam (MEL) significantly alters key biomarkers following blast-induced traumatic brain injury. These analgesics modulate neuroendocrine and neuropathological responses, impacting study interpretations.
Area of Science:
- Neuroscience
- Traumatology
- Pharmacology
Background:
- Blast-induced traumatic brain injury (TBI) is a critical concern, particularly for military personnel.
- The impact of commonly used analgesics on neuroendocrine and neuropathological outcomes after blast exposure is not well understood.
Purpose of the Study:
- To investigate the effects of preinjury buprenorphine (BUP) or meloxicam (MEL) on hypothalamic-pituitary-adrenal (HPA) axis activation, axonal injury, tau phosphorylation, and astroglial responses following blast exposure.
- To assess the modulation of specific biomarkers by these analgesics in a rat model of blast TBI.
Main Methods:
- Male Sprague Dawley rats were subjected to two blast waves (∼19 psi).
- Groups included sham, blast, blast + MEL, and blast + BUP.
- Measurements included serum corticosterone, adrenocorticotropic hormone (ACTH), cerebrospinal fluid (CSF) phosphorylated neurofilament heavy chain (pNFH), and regional protein expression of pNFH, pTau, and glial fibrillary acidic protein (GFAP) at days 1 and 30.
Main Results:
- Blast exposure caused acute elevations in corticosterone, ACTH, and pNFH.
- BUP suppressed both hormones; MEL selectively reduced ACTH.
- Both analgesics attenuated acute pNFH increases, with MEL showing stronger long-term reduction of pNFH and GFAP, indicating reduced axonal and astroglial pathology.
- MEL also provided modest, region-specific reduction in tau hyperphosphorylation.
Conclusions:
- Preinjury analgesics substantially modulate key biomarkers of blast-induced neurotrauma.
- These modulations introduce confounds that can affect cross-study reproducibility and interpretation.
- Findings highlight the importance of considering analgesic effects when interpreting blast TBI biomarker data, suggesting biomarker modulation rather than direct neuroprotection.
